ISSN 1022-7954, Russian Journal of Genetics, 2006, Vol. 42, No. 9, pp. 1053–1065. © Pleiades Publishing, Inc., 2006.

Original Russian Text © B.F. Chadov, 2006, published in Genetika, 2006, Vol. 42, No. 9, pp. 1261–1275.

THEORETICAL PAPERS
AND REVIEWS

A New Stage in the Development

of Genetics and Term Epigenetics1
B. F. Chadov
Institute of Cytology and Genetics, Russian Academy of Sciences, Novosibirsk, 630090 Russia;
fax: (383)333-12-78; e-mail: chadov@bionet.nsc.ru
Received March 22, 2006

Abstract—Genetics requires verification of the notion of gene. In this article, DNA and DNA parts are pro-
posed to be named progenes, while the term gene refers to the informational products produced on DNA. These
are RNA genes, protein genes, and DNA genes (transposable elements). The focus of genetics is switched today
from characters of intraspecies difference to characters of intraspecies similarity. Regulatory genes controlling
ontogeny (ontogenes) become the main object of research. These genes can be isolated by methods of both
reverse and direct genetics. The properties of ontogene mutations, isolated by methods of direct genetics, are
described. The problematic of epigenetics is related to the expression of ontogenes. The term epigenetics is not
correct because of its ambiguity.
DOI: 10.1134/S1022795406090110

INTRODUCTION “higher” than DNA, i.e., probably, the informational

As a rule, the appearance of a novel science or a field
of science is related to the development of a new
method, generating abundant new data. Intellectual
resources of researchers are then spent on processing of
this information, while no attention is paid to relating it
to the previously existing evidence. The new knowl-
edge at first seems alien and poorly connected to the
neighboring areas of knowledge. It becomes necessary
to specifically define the boundaries of the new filed
and to name this field. The name should describe the
field (i.e., be unique) and be in logical connection with
the names of related fields of science. It is clear that the
process of the initial development of a new field of sci-
ence is complex both in essence and in a formal sense.
The word epigenetics has been only recently intro-
duced to genetics. The response of the scientific com-
munity has been ambiguous [1–3]. For some research-
ers, this was a long-awaited signal for parting with not
working (for an unknown reason) statements of classi-
cal genetics; for others, it was simply nonsense. Indeed,
the introduction of this term may be regarded as a for-
mal recognition of the existence of a system of a higher
order (prefix epi means above, higher) above the gener-
ally known genetic system. The genetic system, which
we though governing, turns out to be governed, while
the governing system is the one, of which we know vir-
tually nothing.
For most researchers, who equate gene and DNA,
epigenetics encompasses all that is “above” and
1The terminology and statements made by the author in this article
are of a debatable character.
products, formed on DNA. The issue of defining epige-
netics is further complicated by the existence of term
epigenesis, which appeared long before genetics as a
science [4, 5]. The meaning of epigenesis is not related
to epigenetics, but in terms of syntax epigenetics is a
derivative of epigenesis.
To clarify the essence of epigenetic, we should
sequentially consider the following issues: (1) did a
new branch of genetics, deserving a special name, in
fact emerged; (2) to what extent is the term epigenetics
unique; and (3) how this term is connected with the
names of the neighboring fields of science.
FOUR STAGES IN THE DEVELOPMENT
OF THE NOTION OF ELEMENTARY
HEREDITARY UNIT, OR FOUR STAGES
OF DEVELOPMENT OF GENETICS
The first stage is related to the name of Mendel and
the idea on the existence of discrete material units of
heredity, transmitted from parents to the offspring. The
idea was based on experimentally found rules of inher-
itance of characters. The unit of heredity was termed by
Mendel factor [6]. Later, Bateson and Iohannsen [7, 8]
coined for it the term gene. The word gene, derived
from the Greek genos (kinship, origin) adequately
reflects the essence of the hereditary unit, namely, its
ability to be implemented in a character, “give birth” to
a character. Methodologically, the first stage of genetics
was hybrid analysis.
The second stage in the development of genetics
consisted in an attempt to “materialize” the gene.
According to the chromosomal theory of heredity,

1053
1054
iRNA Proteins
(structural,
tRNA enzymes)
rRNA
microRNA
Fats
Regulatory
DNA proteins
Carbohydrates
Mobile
elements
Cells
Fig. 1. Pathway from the integral hereditary substance
through discrete informational products to final constituents
of the living matter.
advanced by Morgan and his coworkers [9], gene is part
of a chromosome. Methodologically, the second stage
of genetics was cytogenetics (cytological investigation
of chromosomes as carriers of genetic information).
The third stage is related to the discovery of DNA as
a chemical substance, responsible for heredity. This
stage involved the discovery of the DNS structure, the
genetic code, and many other processes, involving
DNA. At this stage, gene was equated to a DNA region
[10]. Genetics proceeded to the molecular level. A large
field of science, molecular genetics, has appeared.
The fourth stage. It seems that the third stage of the
development of genetics as a science is coming to a
close, with genetics entering the fourth stage. At this
stage, informational products, synthesized on DNA,
rather than DNA and its parts, will be regarded as
genes. This issue is directly related to the topic of this
article and thus will be considered in detail.
DNA MOLECULE AND ITS PARTS
ARE THE SUBSTANCE OF HEREDITY
BUT NOT GENES
Historically, the search for the material substrate of
genes was successful twice. The first time the sought
substance was chromosome; the second time, DNA.
These achievements were so significant that some dis-
crepancies and inaccuracies were disregarded. How-
ever, they exist and are the same in both cases.
According to the genetic doctrine, genes are discrete
material units (1), which are transmitted from parents
to offspring via gametes (2). It has been demonstrated
that chromosomes and DNA molecules are transmitted
with gametes, but they are materially integral and,
strictly speaking, cannot be called discrete. Certainly,
the continuous DNA molecule can be divided into
parts, as any other material body, but this does not allow
to consider neither DNA not this body as discrete. In
CHADOV
the process of realizing the genetic information, infor-
mational products, e.g., RNA, are formed on DNA.
These are indeed discrete units. However, they do not
satisfy the second part of the definition of the gene: they
are not transmitted from parents to the progeny (the
exceptions will be discussed below). Thus, “material-
ization” of the gene is not as perfect as seemed earlier.
As in the case of chromosomes, in the case of DNA we
only approached the understanding what is the material
basis of the gene. The history of the appearance and
change of the gene notion in the 20th century was dis-
cussed in detail by Ratner [10].
MOLECULAR GENETICS CREATED
ALL PREREQUISITES FOR REVISING
THE NOTION OF GENE
The ingredients that serve to build living organisms
are organic substances: proteins (structural proteins and
enzymes), fats, carbohydrates, and the cell as a struc-
tural entity. Organic compounds are the chemical mate-
rial of an organism, while enzymes catalyze biochemi-
cal transformations of substances. The cell is a special
entity, which is not synthesized as an organic com-
pound, but is completed during cell division. All of the
above must be built as a result of realizing genetic
information, received by the new individual from the
parents (Fig. 1).
Genetic information is contained in the parental
DNA, but it cannot be realized without mediators. The
mediators form the “information flow,” which starts
with DNA and ends with the production of the final
ingredients (Fig. 1). A role of elementary units that real-
ize the information transfer is played by RNA, regula-
tory proteins, and mobile DNA. They share two com-
mon properties: the presence of information and inde-
pendent behavior.
In the full sense of the word, exactly these products
are genes. They are discrete, contain information, and
transfer it for realization. Hereafter, the original DNA
and its parts are called respectively progenome and
progenies. The phrase hereditary substance is also
appropriate in this respect. Thus, heredity is transmitted
via progenies and realized via genes. This renaming
makes the notion of hereditary units more precise.
Let us group genes into three categories: RNA
genes, protein genes, and DNA genes. The category of
RNA genes includes iRNA, rRNA, microRNA, and
tRNA. The category of protein genes includes regula-
tory proteins and transcriptional factors. DNA genes
include DNA of transposable (mobile) elements (Fig. 2).
In this new interpretation, genes are not universal in
their structure, as was thought before. Universality is
now a property of progenes. However, as shown later,
gene diversity opens new perspectives for solving
genetic problems.
From the viewpoint of epigenetics, the information
products termed here genes are epigenes, while DNA
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9 2006
 A NEW STAGE IN THE DEVELOPMENT OF GENETICS AND TERM EPIGENETICS 1055

(a) (b) Oocyte Zygote Sperm

(a) Genomes

or y Ì p i n‚ ˚ Âg„e
lÎaflt Ú Ó ˚Âr o·Â oÎteÍ Ó Ân Ì
„uÛ ·rÂ

te

e˚
êe g

s
Îi nÍ
A -– R

Ì ˚ –-
sË

–-
DNA DNA (b)
–-
Ñçä Ñçä Progenomes and genes
Nä

„ Âes

D
ÑN
å
êRç

(genes) (progenes)
MÓob·i
(„ÂÌ˚) (ÔÓ„ÂÌ˚)

en

çA
ä- –g

ä-–ge
Ël Îe
–

NçA
Fig. 3. Two schemes of inheritance of hereditary factors.
-

„n
ÂeÌ
˚

tÚs Ì˚
 ˝El Ï ÂenÌ
Î eÂm
Organism
Fig. 2. Spaces of genetics and epigenetics at different mean-
ings of the term gene. (a) Traditional notion of gene as a
DNA region: genetics is shown as the inner circle, epigenet-
ics, as the outer circle; (b) notion of gene as a discrete infor-
mational product: genetics operates with progenes and
genes, epigenetics as an area does not exist.
and its regions are still genes. The modern molecular
genetics showed that tens and hundreds of products
with different functional roles could be produced on the
same DNA region. Since in genetics, gene is a prod-
uct with a certain function, neither the total DNA
molecule nor its segments do not conform to the term
of gene. In addition to the statement on non-discrete-
ness of the DNA molecule, this is another argument
against the regard as genes the DNA molecule or its
regions.
ADVANTAGES OF RENAMING DNA
IN PROGENES AND INFORMATIONAL DNA
PRODUCTS, IN GENES
The above renaming does not leave place for “epi-
genetics,” since the events occurring with genes must
be termed genetic rather than epigenetic (Fig. 2).
The division of a hereditary unit into the progene
and the gene clarifies the process of information trans-
mission from a parent to the progeny, from a dividing
cell to the daughter cells. In each case, a complete num-
ber of progenes (DNA) and a certain gene set are trans-
mitted (Fig. 3). Transmission of genes along with the
hereditary substance assumes the character of a rule.
The maternal and paternal effects in character inherit-
ance [11, 12] and the basic rules of the ontogenetic pro-
cess [13] are explained. Progenes cannot be switched
without genes. Depending of the transmitted genes, the
development may follow different programs. Punctu-
ally following the rule of transmission of “genes along
with progenes,” as discussed further, removes the cover
of mystery from the emergence and the transmission to
the progeny of the “functional states of genetic mate-
rial.”
In the classical sense, the gene combines two func-
tions: transmission of information (passing it to the
progeny) and its realization (the formation of a charac-
Rê s˚
(a) classical scheme: genes are inherited; (b) proposed
–
-
scheme: progenes and genes are inherited.
Organism
ter). It is reasonable to assume that these functions are
fulfilled by two different, albeit mutually connected
carriers: progenies transmit the information and genes
realize it. In the case of classical interpretation of the
term gene, information transmission automatically
implies its realization. Modern genetics cannot assume
such oversimplification. It is known that the activity of
most genes is timed to the particular ontogenetic stages,
while at the other stages these genes are inactive. There
are genes that are active in one individual and inactive
in another. The function of a significant part of trans-
mitted DNA remains unknown.
The above term revision cardinally changes the con-
cept of genetic system. Instead of the classical DNA–
protein chain, a cycle similar to the Eigen’s model is
proposed: DNA–protein–DNA [14, 15]. According to
Eigen’s model, a set of progenes (DNA) cannot inde-
pendently develop into an organism. It can be realized
only in the presence of preliminarily acted genes and a
morphological structure in form of a cell. In each inter-
val of the life, progenes produce structural and regula-
tory proteins. The former build an organism, the latter
determine the activities of some progenes in the follow-
ing life stage. In the case of ontogeny, one of the cycle
stages was named producing a regulatory product “for
export” [13]. The genetic system after Eigen in our case
is a constant interaction between progenes and genes.
This interaction can stop at some life stage, but is
always resumed. Its beginning dates back to the time of
the appearance of life (“the initial jolt”).
The concept of the interaction, of hypercycles at dif-
ferent scales, allows us to expand the horizons of genet-
ics. To date, genetics is not the science on genes “giving
birth” to characters, as it was seen at the previous stage
of the development of genetics, but a science on the
mode of existence of the living matter. Interaction
between genes and progenes for the first time provides
a possibility to recognize the working genetic system of
an organism simultaneously as part of the global bio-
logical life and as part of the ontogeny of the given spe-
cies, and its phylogeny.
In the 20th century, genetics has stimulated the
development of the information theory [10, 16], the the-
ory of dynamic systems [17], and synergetics [18].
However, the theoretical basis of genetics itself was not
considerably changed by the development of these the-

RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9 2006

1056 CHADOV
ories. The subdivision of the informational genetic unit,
the gene, into two units, the gene and the progene, lies
foundation for devising a cyclic gene–progene model.
Based on this model, the modern static genetics can
develop into the dynamic genetics, which would have
all attributes of the dynamic system: connection with
flows of energy, development, generation of informa-
tion, etc. [17].
Recognition of the existence of different gene cate-
gories opens an avenue for studying features of the
action of these genes. Geneticists working with
homeotic genes and other signal genes note low pene-
trance and high lethality of their mutations, as well as
unexpected effects of mutation interactions [19]. In
these aspects, these mutations strikingly differ from
mutations of Mendelian genes. We will not understand
these differences, if we restrict ourselves by studying
differences between primary gene sequences. However,
if we compare the set of genes (in the new meaning)
controlling a Mendelian character, with the set of genes
controlling the formation of a so-called normal charac-
ter, they will be different. Identical as progenes, they
are implemented by different genes.
Structural genes obey the “dominance-recessivity”
rule. This rule holds owing to the mode of interaction
between the final products–structural genes, but not
owing to a particular DNA structure of these progenes.
Mutations of regulatory genes governing development
(ontogenes) are characterized by a different rule, “dom-
inant lethality or the absence of expression” [20]. This
rule is ensured by a special mode of interaction of
homologous protein genes, rather than the final struc-
tural proteins, forming the character at the last stages.
The rules for DNA genes, known as transposable ele-
ments, are strikingly different from that.
MODERN GENETICS HAS STARTED TO STUDY
CHARACTERS OF INTRASPECIES SIMILARITY,
NEGLECTED IN CLASSICAL GENETICS
The revision of the term gene is relevant in context
of the event that has already occurred in genetics, but
has not been adequately appreciated. The contemporary
genetics focuses on biological characters alien to clas-
sical genetics. These are characters of intraspecies sim-
ilarity or, according to the accepted terminology, “nor-
mal characters.” Their formation does not require
defects in the primary DNA structure. It starts earlier
and looks far more complicated than the formation of
Mendelian characters. The formation of a Mendelian
character begins with transcription of a changed DNA
sequence of particular genes. These are structural genes,
activated at the final stages of the normal character for-
mation. The formation of the interspecies similarity
character commences at the zygotic stage and earlier.
Character is all in which objects and phenomena
are similar or in which they differ from one another; an
aspect of an object or phenomenon, by which we can
RUSSIAN JOURNAL OF GENETICS
identify the object or the phenomenon. This is the defi-
nition of the character in formal logics [21]. Characters
inherent only to the given object are called differentiat-
ing and inherent to many objects, shared or non-differ-
entiating [21]. In terms of biological objects, individu-
als within a species have both shared and differentiating
characters. The shared characters form intraspecies
similarity, while differentiating characters, intraspecies
difference(s) [22, 23].
To analyze inheritance of characters, Mendel used
characters of intraspecies difference. These were well
inherited in breeding intra se and represented clearly
distinct character pairs: white and red flower color, yel-
low and green pea color, smooth and wrinkled pea sur-
face, etc. The use of characters of intraspecies differ-
ence was Mendel’s brilliant discovery. Many of his pre-
decessors crossed members of different species to study
inheritance (in some interspecies crosses, first-genera-
tion progeny is viable). Interspecies crosses proved
unsuccessful [24].
Mendel’s choice provided a possibility to observe
the inheritance of a character pair in any number of gen-
erations, while the fact that the bearers of these charac-
ters belonged to the same species removed all problems
connected to crossing. The inheritance of characters of
similarity (at least as an experimental task) was not
studied by Mendel and long time after him. To trace
characters shared by parent in hybrid generation is
meaningless, since they are identical in all past, present,
and future members of the species by definition. Thus,
at its birth genetic virtually was genetics of characters
of intraspecies difference.
After the famous works by Muller, documenting the
appearance of genetic mutations induced by ionizing
radiation [25], the mutational period in the develop-
ment of genetics has started. Many authors generated
numerous mutations in diverse living organisms [26].
Working with mutations has not changed the character
of genetics stated above. Mutant characters were char-
acters of intraspecies difference. Researchers still
worked with pairs of characters, one character being
mutant, and the other, normal. To be more precise, the
normal character was the one that had not been changed
by mutation.
In classical genetics, it was thought that the “norm”
in the mutation–norm pair is the element constituting
“the great norm,” i.e., the organism. Geneticists aimed
at obtaining as many mutations as possible. It was sup-
posed that the issue of the genetic structure of the
organism would be thus resolved automatically. Until
very recently, there was no distinction between charac-
ters of similarity and difference in genetic literature.
Because of this approach, the purpose of the bulk of
genetic material was not understood. This situation has
continued until the present.
Classification of biological characters into two cate-
gories has been made rather recently [22, 23]. It was
supposed that variability of characters of one of the cat-
Vol. 42 No. 9 2006
 A NEW STAGE IN THE DEVELOPMENT OF GENETICS AND TERM EPIGENETICS
egories and the absence of variability in the other cate-
gory masked their different genetic bases. This assump-
tion proved to be true.
CHARACTERS OF INTRASPECIES SIMILARITY
AND AN APPROACH TO THEIR INVESTIGATION
It was supposed that the sought genes constitute the
invariant part of the genome of the species. Altukhov
[27] was the first to advance the concept of the invariant
genome part, developing it at the population level. Our
initial statements were as follows: (1) the genome of the
species has an invariant part; (2) mutations of invariant
genes are dominant lethals; but (3) dominant lethality
of the mutations is not obligate: such mutation can be
lethal in some organisms, but not lethal in other organ-
isms. To put it differently, these dominant lethals
exhibit conditional lethality [28, 29]. The experimental
work was aimed at searching for conditional dominant
lethal mutations. Using methods devised for this pur-
pose [28–30], about 100 mutations were found, but this
number can be easily increased.
A rule for choosing a character for genetic work,
introduced by Mendel, was taking characters with sta-
ble expression (expressivity) and stable inheritance in a
pure line (penetrance). Characters that do not vary in all
individuals of the species are thought “the best.” This
rule is based on an idea that gene is a stable elementary
unit of heredity that is not affected by variation in exter-
nal and internal factors. The protocol for character
selection, formulated by Mendel, was aimed at separat-
ing true (genetically based) characters from unstable
(not genetically based), externally determined ones.
The above procedure of selecting conditional dominant
lethals rejects this attitude, introducing another one:
there is a category of genes that do not necessarily man-
ifest in all members of the species.
ONTOGENES AND THEIR PROPERTIES
The uniqueness of the genetic basis of characters of
intraspecies similarity followed from the unusual prop-
erties of the obtained mutations.
Morphoses in the progeny of the mutants; introduc-
ing the term ontogen. In the progeny of mutant individ-
uals, individuals with visual defects (morphoses) usu-
ally appear at frequencies ranging from several percent
to several tens percent [13, 31]. Morphoses can affect
any parts of an individual, but usually at one side, right
or left. They include defects of type “plus tissue” (pro-
trusions, additional legs, wings, thoracic parts, etc.) or
“minus tissue” (absent leg, wing, eye, part of the head,
etc.) (Fig. 4). Such examples of pronounced morphoses
as two heads, an additional leg, three wings suggest that
morphoses are caused by a switch of a subprogram of
the normal development in an inadequate cell group. As
the mutated genes clearly are related to the process of
ontogeny control, they were named ontogenes. In devel-
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9
1057
opmental genetics, they seem to be close to newly
appeared notions of signal genes and key genes [32, 33].
A mutation in an ontogene change its manifestation
depending on the genetic background (sex of the muta-
tion donor, genotype of the partner, sex of the mutation
recipient, genotype of the mutation recipient). Accord-
ing to conditions of isolation, the mutations were
expressed as lethal in one genotype and lacked this
expression in another one. All genetic conditions listed
in the heading of this section were present in the muta-
tion isolation procedure [28, 30].
A mutation in an ontogene changes its expression
depending on the spatial position of the genetic mate-
rial in the cell. Mutations dealt with in genetics are usu-
ally indifferent to the position of the mutant region in
the nucleus as well as to the positions of other regions.
These mutations are maintained in lines, carrying
diverse chromosomal rearrangements, and do not lose
their standard expression. The lethal mutations
described above proved to be sensitive to chromosomal
rearrangements in the genome [12, 34]. In genotypes
with rearrangements, they ceased to be lethal. The rear-
rangements preserved their effect in the progeny even
in the cases when the rearrangement was carried by the
mother rather than the progeny (the maternal effect of a
chromosomal rearrangement) [12].
A mutation in an ontogene results in genetic insta-
bility. The above mutations manifested another prop-
erty that distinguished them from Mendelian genes. A
mutation in an ontogene induced instability in the
genome. We described seven different manifestations
of such instability [35], some of which are considered
below.
While maintained in laboratory cultures, ontogene
mutations lose their lethal expression in the genetic
background, in which they manifested it previously.
The presence of an ontogene mutation disturbs the pro-
cess of cell division, both mitotic and meiotic. In meio-
sis, nondisjunction and loss of X chromosomes occur.
The rate of chromosome loss reach tens percent. In
somatic cells (mitosis), the chromosome loss is mani-
fested in the appearance of mosaic individuals and
gynandromorphs (individuals having traits of both
sexes).
Instability is also expressed in secondary mutagene-
sis. Periodically, in the mutant progeny, visible muta-
tions appear singly, in groups, or sometimes sequen-
tially in consecutive generations. Another characteristic
feature of ontogene mutant cultures is the presence of
modifications. Modification is an exterior defect,
which, in contrast to mutation, is not preserved over
generations. The formation of morphoses discussed
above can also be considered as a manifestation of
instability. The phenomenon of genetic instability has
been known [36]. In the present work, it was found that
this phenomenon is caused by mutation in a special
gene, ontogene.
2006
1058
Fig. 4. Morphoses in Drosophila melanogaster. Top row (from left to right): additional thorax with wing, filaments in place of right
wing, additional wing at left (directed forward); bottom row (from left to right): additional wing as a haltere, “hanging” eye, absence
of several tergites.
Manifold manifestation of the ontogene mutation.
Mendel classified genes into dominant and recessive.
The currently existing genetic mutations are also subdi-
vided into recessive and dominant. Mutations of onto-
genes are recessive and dominant simultaneously. In
some crosses, they behave as dominant lethals. In labo-
ratory cultures, they are maintained in heterozygotes as
typical recessive lethals. Some of them have visible
recessive expression in homozygotes. These are dimor-
phic mutations with different expression in males and
females [31]. Presumably, ontogenes are DNA
sequences, from which several genes with different
functions are transcribed. Some of these genes are
structural, others are regulatory. The former are reces-
sive, and the latter, dominant.
Figure 5 schematically shows that ontogenes are
regulatory genes connected by their signal function in
regulatory networks. Structural genes, albeit tran-
scribed from the same DNA sequences, does not form
such networks. DNA damage, depending on its position
in the gene locus, may cause: (1) a structural gene
CHADOV
defect only, (2) a regulatory ontogene defect only, and
(3) a defect in both genes. In the first case, the defect
will be expressed as a typical Mendelian mutation; in
the second, as an ontogene mutation (conditional dom-
inant lethal); in the third, as a Mendelian mutation with
abnormal inheritance, conditional lethal effect, interac-
tion with other genes.
The listed above mutation properties are strikingly
exotic, although the mutations were generated by
means of a traditional irradiation procedure and are
inherited as defects of the primary DNA structure. They
combine many of enigmatic phenomena that sporadi-
cally appear in genetic experiments. These include
incomplete penetrance, modifications, morphoses, and
instability. These phenomena are often interpreted as
cases of epigenetic [1, 37], dynamic variation [38] and
attributed to noncanonical heredity [39]. However, in
our experiments, they were all caused by trivial radia-
tion damage of DNA.
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9 2006
 A NEW STAGE IN THE DEVELOPMENT OF GENETICS AND TERM EPIGENETICS
GENETIC BASES OF MENDELIAN CHARACTER
AND CHARACTER OF INTRASPECIES
SIMILARITY ARE DIFFERENT
Based on the evidence of the existence of two gene
categories, one of which is ontogenes (regulatory genes
controlling ontogeny), the course of ontogeny is sche-
matically presented in Fig. 6. Ontogenes form a multi-
level network. Structural genes are located at the ends
of the regulatory chains. The process of ontogeny is
based on the principle of relay. An activity signal,
arisen in a zygote, passes through the ontogene chains
to the structural genes. After transmission of the signal,
the ontogene switches off, but the activity of the struc-
tural genes is preserved (Fig. 6, right) [31]. The signal
transmission is connected to cell division, ensuring the
formation of differentiated groups of cells in a multicel-
lular organism [13].
According to this scheme, characters of intraspecies
differences appear as a result of mutations of the struc-
tural genes at the chain ends. The characters, as a rule,
are monogenic. These are characters of intraspecies dif-
ferences, existing in nature, and numerous artificially
produced characters (mutations). Only to date we can
understand that the fundamental Mendelian principle of
discrete heredity could be formulated only by analysis
of characters of intraspecies differences. Genes control-
ling these characters are located at the ends of the func-
tional gene chains, and therefore are mutually indepen-
dent. The genetic nature of the characters of intraspe-
cies similarity is different: these are total blocks of
hierarchically connected ontogenes, ending by many
structural genes. Thus, although the characters are con-
trolled by genes, the genetic bases of these characters
are different.
The above scheme shows that every gene is not
matched by a phene (visible manifestation). A mutation
in a structural gene probably will produce a definite and
heritable phenotypic change. A mutation in an onto-
gene, which is an element of a regulatory chain, will
disrupt the development (lethal action). The organism
simply will not exist. A mutation in an ontogene can
lack manifestation, because this mutation is a condi-
tional lethal.
The above scheme evidently does not reflect ontog-
eny in all its complexity. Even small stages of this pro-
cess, studied experimentally, look far more intricate
[33]. However, even this simple scheme clearly shows
that the character in Mendelian and classical sense is a
defect of development, caused by a defect in the DNA
sequence. Rimane was right when he ironically referred
to collections of genetic mutations as “a real home for
disabled” [40]. The characters of intraspecies similarity
appear as a result of realization of long gene chains. To
form such a character, no defect in the DNA sequence
is required. In connection with the chain process of for-
mation of a normal character, including operation of
regulatory ontogenes, features of the genetic system
that could not be found by classic hybrid analysis
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9
1059
A B C
Structural
protein
Regulatory
protein
Gene A Gene B Gene C
Fig. 5. Polygenic effect of a mutation, disrupting the DNA
sequence, which undergoes alternative splicing. Changes in
the sites of initiation and termination of transcription
(arrows) of progenes A and B, four proteins appear for each
gene. Progene C produces three proteins. One protein of
each set (top) is structural, the remaining ones are regula-
tory. The regulatory proteins are involved in regulatory
pathways. The functional associations between them are
shown as lines. If the DNA is damaged (progene A
sequences), all four proteins (structural and three regulatory
ones) are changed, which results in complex phenotypic
expression and unusual inheritance of the mutation.
appear. They become accessible only as a result of the
development of methods of reverse genetics and novel
methods of hybrid analysis, devised only recently (see
above).
Figure 7 presents pathways of realization of heredi-
tary information in the case of a Mendelian character
and a character of intraspecies similarity. In the first
case, it is a short chain: progene–RNA gene–structural
protein; in the second, a cascade, consisting of many
chains: progene–RNA gene–protein gene (transcription
factor), connected by the bond protein gene–progene
(numerals 1, 4, 7). Complex variants involving
microRNA and DNA genes (transposable elements) are
not presented in the scheme.
In the case of a Mendelian gene, the features of its
inheritance are explained by the relationships between
two final structural genes: the normal and the defective
one. These relationships, known as recessive–domi-
nant, were described by Mendel. In the case of the char-
acter of intraspecies similarity, a protein gene–progene
(=transcription factor–DNA) stage is multiply wedged
in between. The relationships between two protein
genes, one of which is normal and the other, defective,
are still unclear. Experiments with conditional domi-
nant lethals suggest that these relationships are differ-
ent from the classical recessivity–dominance scheme.
In most cases studied, the presence of a defective prod-
uct even in one dose is lethal. Not considering more
complex cases of the cascade chain, it is clear that
genetics of similarity characters must be full of sur-
prises.
2006
1060 CHADOV

(a) (b)
t4

t3

t2

t1

t0

Fig. 6. Genetic model of ontogeny [31]. (a) Genes and signaling pathways. The genome of an individual consists of structural genes
(dark circles) and ontogenes of various ranks (open circles, squares, and triangles). The ontogene is represented by a number of cis-
alleles (signs divided into sectors). t0–t4 are ontogenetic stages. The genome activation proceeds by system of signaling pathways
(lines connecting genes, arrows). The signal pathways are terminated by inclusion of structural genes. Ontogeny is the process of
sequential switching of regulatory genes of different ranks according to the relay principle. In transition from the previous to the
subsequent ontogenetic stage, the ontogenes acting at the previous stage, as well as structural genes providing the appearance of
presumptive structures (hatched circles) are switched off. (b) Ontogeny at one of the last stages (t4). Switched off genes are shown
by hatched lines. Most of the structural genes and some ontogenes with similar time of switching (regulatory genes of stem cells)
remain switched.

GENETIC SYSTEM AND THE IMPACT
OF THE EXTERNAL AND THE INTERNAL
ENVIRONMENT
Variability of structural genes and variation of onto-
genes are provided by different mechanisms. The
former is based on the existence of viable variants of
the primary DNA structure, known as alleles. In Fig. 8,
they are shown as dashed circles. A diploid organism
has two alleles of each gene, one in the maternal, and
the other in the paternal chromosome. The remaining
alleles are carried by other individuals of the same spe-
cies. Variability of such a species is of the populational
nature.
Variability of ontogenes is genomic rather than pop-
ulation one. Each ontogene is represented by a cassette
of alleles. Variation emerges, because the regulatory
pathway of several ontogenes may pass through differ-
ent cis-alleles of these genes. With many ontogenes and
many cis-alleles of each ontogene, the number of vari-
ants is enormous. This type of variation is not con-
nected with changes in the primary DNA sequence. It is
likely that variation of this type causes the so-called
ontogenetic variability [41, 42], in particular, bilateral
asymmetry [43].
This type of variation by meaning coincides with
epigenetic variation, related to gene activity/inactivity.
In our case, we focus on the possibility of this variation
type, rather than on the activity of the target genes. This
variation is caused by the existence of cis-alleles, each
of which is capable of performing the function.
The cis-allelic organization of ontogenes creates
conditions in the organism for ontogenetic variants, i.e.,
programs and subprograms of different levels of com-
plexity. The most grandiose of them is the sexual pro-
gram, which operates in two variants, male and female.
With practically identical sets of operating structural
genes, the difference between the male and the female
organisms, caused by different ensembles of regulatory
genes, is striking.
Analysis of operation of an ontogene system (gene
network, in Kolchanov’s terminology) allows us to
approach the gene–environment problem, which
repeatedly caused confrontation between biologists and
geneticists. In the work of a regulatory system, the
notion of signal is significant. In genetics, this is a
material product activating a gene. In the case of sex
determination, the signal for switching the male or the
female developmental pathway is genetic. It is either
the presence of the Y chromosome, or the ration

RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9 2006

 A NEW STAGE IN THE DEVELOPMENT OF GENETICS AND TERM EPIGENETICS
between the number of sex chromosomes and auto-
somes. It was repeatedly suggested that factors of inter-
nal (positional ontogenetic information) and external
environments might serve as signals. In plants, striking
examples of external signals changing developmental
programs are known. For instance, in water buttercup,
the aerial environment results in the development of
arrow-shaped leaves, while in the water environment
the leaves are stripe-like. For cultured plants, the theory
of alteration of limiting ontogenetic factors is sup-
ported by experimental facts. According to this theory,
the ontogeny may take different pathways, i.e., involve
different genes, depending on the signal from the envi-
ronment, received at a particular time [44, 45].
If we take a suddenly arisen variant of ontogeny for
an acquired character, it may prove to be inherited,
which in fact is not surprising. However, this character
will be expressed only under conditions that led to its
expression in the parent. The phenomenon of morpho-
ses in the progeny of ontogene mutants is very instruc-
tive for understanding inheritance of acquired charac-
ters. First, the entity that we call the acquired character
has an intricate structure. Protrusions in the form of a
leg, arista, tergite part, etc., are doubtlessly a result of
realization of part of the genetic program of ontogeny,
albeit they are realized in inappropriate places. Their
repeated manifestation cannot be excluded, since the
program itself is heritable. Generally speaking, the
acquired character (if it is not a deformity) cannot be
without a genetic basis. If so, a progeny, receiving from
a parent its genome, theoretically inherits the possibil-
ity of expressing this character. This absolutely does
not require transmission of information from somatic to
germline cells, as is sometimes supposed [2].
In my opinion, there is also a channel for direct
effect of the environment on the genetic structure of an
organism. This occurs in the period of genome destruc-
tion and reorganization [35]. In these periods, such
variants of the developmental programs and subpro-
grams must be used, which ensure maximum possible
adaptation of the organism in the given environment. If
the system rearrangement proves to be successful, then
clearly adaptive variants, during which it occurred, will
be incorporated into the new system as an obligatory
element. Thus, the impact of the environment will be
retained by the genetic system, though this process is
more complex than seemed to biologists in the 17th–
18th centuries. This suggestion can be experimentally
tested on mutant lines expressing genetic instability.
A NEW FIELD HAS INDEED APPEARED
IN GENETICS, BUT THE TERM EPIGENETICS
IS INAPPROPRIATE FOR IT
The key idea of the above is as follows: to date
genetics is investigation of “production” of genes on
the progene template before, after, and during the pro-
cess of ontogeny. All processes here are genetic. Refer-
ring to them as epigenetic is incorrect from all view-
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9
1061
Structural Structural Structural
protein 1 protein 2 protein 3
RNA-gene 1 RNA-gene 3 RNA-gene 5
Progene A Progene B Progene C
2 5
1 4 7
RNA-gene 2 RNA-gene 4
3 6
Protein Protein
gene 1 gene 2
Fig. 7. Two pathways of realizing the hereditary informa-
tion of the progenome: short (progene–RNA-gene–struc-
tural protein) and long (regulatory cascade). The cascade
involves protein genes. The regulatory cascade transmits
information by stages from 1 to 7. Boxed are the stable cell
components: DNA (progenes) and structural proteins; in
ovals, short-lived components: RNA-genes and protein
genes.
points, and primarily because the meaning of the term
epigenesis is, strange as it may seem, rather “antige-
netic.”
In Antiquity, the scientific formulation of the idea of
development was represented by two concepts: Plato’s
(“development after a pattern”) and Aristotle’s (“epi-
genesis”). In the first concept, the development is
implementation of a preexisting plan (“thing in itself”);
in the second, as a self-realization process, i.e., the
appearance from unorganized matter (chaos), reorgani-
zation and complication via making a superstructure
(epigenesis) [5]. In the 18th-century biology, these con-
cepts were retained in form of preformism and Wolf’s
epigenesis(cited from [4]). Thus, the word epigenesis
with a quite distinct meaning has appeared and existed
long before the foundation of genetics and coining the
genetic terminology.
Mendelian genetics, classical genetics, and modern
genetics continue the preformism line in the issues of
individual development. The organism is a result of
realization of a hereditary program, consisting of ele-
mentary stable units, genes. At its birth, the ideology of
genetics was straightforwardly preformistic: “a phene
for each gene.” As the science of genetics developed,
the issue of the origin of the character tilted toward epi-
genesis. Morgan [46] admitted change and develop-
ment of genes during ontogeny; Goldschmidt [47] sug-
gested interactions among gene products not controlled
by genes. In 1963, Mayr [48] wrote that our notions of
the connection between the gene and the character had
been thoroughly revised, with phenotype increasingly
regarded not as a mosaic of separate characters con-
2006
1062 CHADOV

Genes A B C D E F G
E6
E5
C8 E4 F8
C7 E3 F7
Maternal
homolog A1 A2 A3 A4 A5 B1 B2 B3 B4 B5 B6 C1 D1 D2 D3 D4 E1 F1 G1 G2 G3
a

b
Paternal A1 A2 A3 A4 A5 B1 B2 B3 B4 B5 B6 C2 D1 D2 D3 D4 E2 F2 G1 G2 G3
homolog C3 E7 F3
C4 E8 F4
C5 F5
C6 F6

Fig. 8. Scheme of organization and action of ontogenes [34]. C, E, F (dots) are unique structural genes; there are alleles of these
genes in the population (e.g., ë1–ë6), but the diploid genome has only two alleles. Ontogenes A, B, D, G consist of cassettes of cis-
alleles (e.g., Ä1–Ä5). In a concrete organism, only one cis-allele of an ontogene and only in one of the homologs (hatched) is work-
ing. Depending on switching of a cis-allele, a concrete variant is realized. a (hatched line) and b (solid line) are variants of the ontog-
eny. Instead of operating in norm cis-allele Ä1, cis-allele Ä5 may be activated. Mutation in cis-allele D4 upon development by vari-
ant b is lethal, but is not expressed in development by variant a.

trolled by genes, but as a final product of a complex
interacting system, an epigenotype.
Waddington [49, 50] aimed at uniting genetics and
developmental biology, but according to him, ontogeny
was not a process entirely controlled by genes [50,
p. 17]. This motivated this author to look for a term to
define the process of individual development without
referring to the term developmental genetics, which
implies genetic basis of ontogeny.
“Several years ago, writes Waddington, I have
introduced the term epigenetics, deriving it from
Aristotle’s epigenesis, the word that is almost
obsolete, and proposed to name epigenetics the
branch of biology studying causal relationships
between genes and their products, which form
the phenotype. This term is currently rather often
used exactly in this sense, but unfortunately, it
turned out to be very appealing, so some authors
employ it to denote very different notions
[…] in my view, we may escape much misunder-
standing, if we reserve this term for the science
studying causal relationships in development, as
was suggested from the very beginning” [51].
The author speaks of phenotype as an epigenetic
phenomenon; he considers cell differentiation and mor-
phogenesis as “elementary processes of epigenetics”
[51].
In other words, for Waddington epigenetics is the
science on the implementation of the phenotype as the
integral realization of the genotype (in modern terms,
the genome) as opposed to the simplistic notion “geno-
type is the sum of genes and phenotype is the sum of
their phenes.” In modern terms, epigenetics deals with
genetic of individual development.
Criticisms considered in Introductions can be
applied to Waddington’s term epigenetics, notwith-
standing insights into the meaning that this author put
into it. By definition, genetics is the science that studies
inheritance of characters. It deals also with the develop-
ment of characters from the hereditary substance. It was
not for nothing that the elementary units of heredity
were named genes. Because of the prefix epi, the term
epigenetics seem to imply something beyond genes and
characters. As noted Waddington [50, p. 38] himself, a
term should not be ambiguous. This is very true. Exactly
for this reason, the term epigenetics is not acceptable.
Aristotle’s notion of epigenesis proved to be unsuit-
able for describing the process of individual develop-
ment. Neither Wolf in the pre-genetic stage of biology,
nor Waddington in the golden age of genetics could
make this description. According to the contemporary
evidence, the ontogeny strictly follows a genetic plan.
Wolf could not know it; even Waddington was not fully
aware of it. In his time, genetics operated only with
structural genes; studies of regulatory genes, at that
only in prokaryotes, have just started.
From the beginning, epigenesis stood against pre-
formism. After the appearance of genetics, which con-
tinued the ideology of preformism, the term epigenetics
emerged in the cases, when researchers encountered
phenomen that could not be explained genetically, i.e.,
on the basis of existence of governing (genetic) units.
In the 1970s, Tchuraev has developed the notion of
epigene. According to Tchuraev, “epigene is a heredi-
tary unit (cyclic system of genes) that has at least two
regimes of functioning of the genes governed by it and
capable of preserve each of the regimes in consecutive
generations” [52, 53]. DNA molecules, consisting of
genes, store information in the structural way, whereas
epigenes do it in the dynamic way [52]. Epigene is a
supergene structure, united by an integral functional
state.

RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9 2006

 A NEW STAGE IN THE DEVELOPMENT OF GENETICS AND TERM EPIGENETICS
Genes in the epigene are DNA segments, whose
activity is maintained by the gene products [54]. Epi-
gene consists at least of two genes. In our terminology,
this concerns interaction of genes and progenes. This
interaction is a typical phenomenon occurring in the
living organism, which has the form of a cycle of a cer-
tain size [15].
The development of the ides of gene systems with
account of their functional state (activity and inactivity)
by Tchuraev as early as in the 1970s was certainly a
great achievement. The author has introduced the
notion on a dynamic way of storing information and the
possibility of inheritance of such information. Based on
epigenes, the noncanonical theory of heredity was con-
structed [39, 52]. Tchuraev argues that the functional
state of a genetic system can be transmitted to the prog-
eny. Hereditary transmission of the functional states of
the parental genome may serve as a basis for serious
consideration of the idea of inheritance of acquired
characters [38, 39].
I believe that the issue on the existence of dynamic
inheritance was influenced by the aforementioned
drawback of classical genetics. Classical genetics is
concerned with genes, but not their products. If, in the
case of Tchuraev’s epigene, we fail to take into account
that the maintenance of the functional state requires
corresponding gene products, the coincidence of the
functional gene state in the parent and the progeny
could be taken for inheritance of dynamic information.
In reality, the functional state is restore, rather than
inherited. The restoration results from the transmission
of a regulatory product. Switching the activity of the
corresponding gene, together with the maternal DNA.
The author himself states so in one of his latest studies
[54]. The renaming of the informational gene products
into genes allows one not to overlook gene products
when considering a functioning genetic system, and
thus to describe the system clearly and comprehen-
sively. If this is done, the number of cases of “transmis-
sion of functional states” from parents to the progeny
must drastically drop.
The word epigenetics is spreading in scientific liter-
ature with an astounding speed, demonstrating an
example of reproduction of replicators of the mem type
(mem is an abbreviation of the Greek word mimos,
which means imitation) (cited from [55, p. 66]). To
date, the bulk of experimental data, ascribed to epige-
netics, should be separated from the term (or candidate
term) itself. If the experimental data on epigenetics are
reliable to the same extent as other data, then the term
epigenetics is debatable. The main objection against the
introduction of the word epigenetics to genetic usage
was formulated in Introduction. It is Waddington, the
author of the term epigenetics, who said: “A term
should not introduce to science any unwanted, addi-
tional meanings, which it might contain in its daily use,
its biological significance should strictly correspond to
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9
1063
the properties that are found in the phenomenon exam-
ined, and to nothing else” [50].
Epigenetics, which was formerly employed as a
term for genetics of ontogeny, is currently assuming
another meaning. Epigenetics begins to include phe-
nomena and processes that classical genetics does not
know of, cannot explain or have not dealt with. The
range of these phenomena and processes is broad, but
they all concern a new class of genes, regulatory genes
controlling development (ontogenes, in our terminol-
ogy). The properties of these genes were discussed in
the first part of this paper. The fundamental to epigenet-
ics is the term epigenetic variation. In contrast to
genetic variation, based on alteration of the primary
DNA sequence, epigenetic variation is a change in the
genome activity pattern. It is related to gene activation
and deactivation, but not to a change in the DNA
sequence. The activity pattern changed during ontog-
eny (which has long been known), and varies among
the individuals within the species, which are at the
same developmental stage (see above about the activity
of cis-alleles of ontogenes).
Two aspects of the activity are of particular interest.
One of them lies in the fact that the transcriptional
activity of a given DNA region does not mean produc-
tion of the same product (see section Manifold Mani-
festations of Ontogene Mutations"); the second, that
there are pattern variants (see section Genetic System
and the Impact of the External and Internal Environ-
ments). It can be seen that within genetics of develop-
ment, an area of general genetic interest emerges,
which is above the concrete problems of ontogeny, i.e.,
morphogenesis, determination, differentiation, etc.
I think that epigenetic is ultimately investigation of
ontogenes. Even now, it is clear that ontogenes are
related to (1) characters of intraspecies similarity (i.e.,
“normal” characters); (2) the process of ontogeny;
(3) switching on and off the gene activity; (4) gene
silencing; (5) parental effects; (6) incomplete penetrance;
(7) dependence of the activity on the location within the
genome; (8) alternative developmental programs; (9)
association of the gene activity with external and internal
environments; (10) speciation [29, 35, 56, 57].
In my view, instead of employing the term epigenet-
ics, one should use the term genetics of within-species
similarity and the term gene in its new meaning. The
revision of the gene notion is inevitable, but will occur
slowly because of clinging to tradition. Instead, we
should develop a more logically formulated genetic
doctrine and a larger field of science named genetics.
Aristotle’s epigenesis, which is in focus of interest of
theoreticians [58, 59], has its place also in traditional
biology. It lies in the field, in biology referred to as phy-
logeny. This issue is beyond the scope of the present
article and will be considered in forthcoming studies.
2006
1064
ACKNOWLEDGMENTS
I thank S.I. Maletskii and E.V. Levites for stimulat-
ing discussion on the issue of epigenetics, as well as
E.V. Razin and I.F. Zhimulev for invitation to collective
discussions of this problem in the framework of the
Russian Academy of Natural Sciences and Vavilov
Society of Geneticists and Breeders.
The work was supported by the Russian Foundation
for Fundamental Research (grant no. 04-04-48100) and
by the Program of the Russian Academy of Sciences
“The Origin and Evolution of the Biosphere.”
REFERENCES
1. Maletskii, S.I., Epigenetika rastenii (sbornik nauchnykh
trudov) (Epigenetics of Plants: Collection of Scientific
Works), Novosibirsk: Inst. Tsitol. Genet. SO RAN,
2005.
2. Korochkin, L.I., On Epigenetics, Evolyutsionnaya biolo-
giya (Evolutionary Biology), Stegnii, V.N., Ed., Tomsk:
Tomsk. Gos. Univ., 2005, vol. 3.
3. Voloshina, M.A., Hierarchy of Genetic Programs and
Evolution, Filosofiya Nauki, 2005, no. 3, pp. 115–126.
4. Zhimulev, I.F., Obshchaya i molekulyarnaya genetika
(General and Molecular Genetics), Novosibirsk:
Novosib. Univ., 2002.
5. Maletskii, S.I., Evolyutsionnaya biologiya. Slovar’ ter-
minov (Evolutionary Biology: Dictionary of Terms),
Novosibirsk: Inst. Tsitol. Genet. SO RAN, 2005.
6. Mendel, G., Versuche uber Pflanzen Hybriden, Verhand-
lungen des naturforschenden Vereins in Brunn, 1865,
vol. 4, pp. 3–47.
7. Bateson, W., The Progress of Genetics since the Rediscov-
ery of Mendel’s Paper, Progr. Rei. Bot., 1907, vol. I, p. 368.
8. Johannsen, W., Elemente der Erblichkeitslehre, Jena:
Fischer, 1909.
9. Morgan, T.H., Bridges, C.B., and Sturtevant, A.H.,
The Genetics of Drosophila: Bibliographia Genetica II,
'S-Gravenhage Martinus Nijhoff, 1925.
10. Ratner, V.A., Genetika, molekulyarnaya kibernetika:
Lichnosti i problemy (Genetics, Molecular Cybernetics:
Persons and Problems), Novosibirsk: Nauka, 2002.
11. Ashburner, M., Drosophila: A Laboratory Handbook,
New York: Cold Spring Harbor Lab., 1989.
12. Chadov, B.F., Chadova, E.V., Khotskina, E.A., et al., The
Main Effect of Chromosomal Rearrangement is Chang-
ing the Action of Regulatory Genes, Rus. J. Genet.,
2004, vol. 40, no. 7, pp. 723–731.
13. Chadov, B.F. and Fedorova, N.B., Elementary Event of
Ontogeny, Dokl. Ros. Akad. Nauk, 2003, vol. 389, no. 3,
pp. 408–412 .
14. Eigen, M., Samoorganizatsiya materii i evolyutsiya bio-
logicheskikh makromolekul (Self-Organization of Mat-
ter and Evolution of Biological Macromolecules), Mos-
cow: Mir, 1973.
15. Eigen, M. and Schuster, P., The Hypercycle, Berlin:
Springer, 1979.
16. Korogodin, V.I. and Korogodina, V.L., Informatsiya kak
osnova zhizni (Information as the Basis of Life), Dubna:
Feniks, 2000.
CHADOV
17. Chernavskii, D.S. and Chernavskaya, N.M., Generation
of Valuable Information, Sovremennye problemy radio-
biologii, radioekologii i evolyutsii (Current Problems of
Radiobiology, Radioecology, and Evolution), Korogo-
din, V.I., Ed., Dubna: Ob. Inst. Yad. Issled., 2001.
18. Chernavskii, D.S., Sinergetika i informatsiya (Synerget-
ics and Information), Moscow: Znanie, 1990.
19. Ivanov, V.I., Interaction of Genes Controlling the Pro-
cesses of Cell Determination, Teoreticheskie problemy
meditsinskoi genetiki (Theoretical Problems of Medical
Genetics), Moscow, 1979.
20. Chadov, B.F., The “Image” of the Regulatory Gene in
Experiments with Drosophila, Rus. J. Genet., 2002,
vol. 38, no. 7, pp. 725–734.
21. Kondakov, N.I., Logicheskii slovar’–spravochnik (Logi-
cal Dictionary–Handbook), Moscow: Nauka, 1975.
22. Chadov, B.F., Chadova, E.V., Kopyl, S.A., et al., From
Genetics of Intraspecific Differences to Genetics of
Intraspecific Similarity, Russ. J. Genet., 2004, vol. 40,
no. 9, pp. 945–948.
23. Chadov, B.F., Characters of Intraspecific Similarity and
the Features of Mendelian Approach to Studying Hered-
ity, Filosofiya Nauki, 2005, no. 3, pp. 94–114.
24. Gaisinovich, A.E., Zarozhdenie i razvitie genetiki (The
Emergence and Development of Genetics), Moscow:
Nauka, 1988.
25. Mfiller, H., The Problem of Gene Variability, H. Mfiller:
Izbrannye raboty po genetike (H. Mfiller: Selected
Works in Genetics), Vavilov, N.I., Ed., Moscow:
Sel’khozizdat, 1937.
26. Auerbach, Ch., Problemy mutageneza (Problems of
Mutagenesis), Moscow: Mir, 1978.
27. Altukhov, Yu.P., Geneticheskie protsessy v populyatsiyakh
(Genetic Processes in Populations), Moscow: Aka-
demkniga, 2003.
28. Chadov, B.F., Chadova, E.V., Kopyl, S.A., and Fedo-
rova, N.B., A Novel Class of Mutations in Drosophila
melanogaster, Dokl. Ros. Akad. Nauk, 2000, vol. 373,
no. 5, pp. 714–717.
29. Chadov, B.F., Mutations Capable of Inducing Specia-
tion, Evolyutsionnaya biologiya (Evolutionary Biology),
Stegnii, V.N., Ed., Tomsk: Tomsk. Gos. Univ., 2001,
vol. 1, pp. 138–162.
30. Chadov, B.F., Chadova, E.V., Kopyl, S.A., and Fedo-
rova, N.B., Delayed Activation of the Maternal Genome
in Early Development of Drosophila, Dokl. Ros. Akad.
Nauk, 2001, vol. 378, no. 6, pp. 841–845.
31. Chadov, B.F., Chadova, E.V., Kopyl, S.A., et al., Genes
Controlling Ontogeny: Morphoses, Phenocopies,
Dimorphs, and Other Visible Manifestations of Mutant
Genes, Rus. J. Genet., 2004, vol. 40, no. 3, pp. 271–281.
32. Korochkin, L.I., Vvedenie v genetiku razvitiya (Introduc-
tion to Development Genetics), Moscow: Nauka, 1999.
33. Davidson, E.H., Rast, J.P., Oliveri, P., et al., A Genomic
Regulatory Network for Development, Science, 2002,
vol. 295, pp. 1669–1678.
34. Fedorova, N.B., Khotskina, E.A., Mitrenina, E.Yu., and
Chadov, B.F., Chromosomal Rearrangements and Specia-
tion: Explanation of Association between the Events,
Evolyutsionnaya biologiya (Evolutionary Biology), Steg-
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9 2006
 A NEW STAGE IN THE DEVELOPMENT OF GENETICS AND TERM EPIGENETICS
niy, V.N., Ed., Tomsk: Tomsk. Gos. Univ., 2005, vol. 3,
pp. 107–120.
35. Chadov, B.F., Chadova, E.V., Khotskina, N.B., and
Fedorova, N.B., Mutation in Ontogenes—Genome
Destabilization—Speciation, Evolyutsionnaya biologiya
(Evolutionary Biology), Stegniy, V.N., Ed., Tomsk:
Tomsk. Gos. Univ., 2005, pp. 92–106.
36. Khesin, R.B., Nepostoyanstvo Genoma (Genomic Insta-
bility), Moscow: Nauka, 1984.
37. Vysotskii, D.L., Elementy biologicheskikh kontseptsii
(Elements of the Biological Paradigm), Novosibirsk:
Nauka, 2004.
38. Golubovsky, M.D. and Churaev, R.N., Dynamic Hered-
ity and Epigenes, Priroda, 1997, no. 4, pp. 16–25.
39. Golubovsky, M.D., Noncanonical Hereditary Changes,
Priroda, 2001, no. 9, pp. 3–8.
40. Khossfeld, U., Yunker, T., Tsakhos, F., and Razran, L.,
Zoologist Adolf Rimane and His Views on Biological
Evolution, Evolyutsionnaya biologii: istoriya i teoriya
(Evolutionary Biology: History and Theory), issue 2,
Kolchinskii, E.I. and Popov, I.Yu., Eds., St. Petersburg,
2003.
41. Astaurov, B.L., The Results of My Research Work in
Genetics, Istoriya biologicheskikh issledovanii (The
History of Biological Studies), Moscow: Nauka, 1978,
pp. 116–159.
42. Strunnikov, V.A. and Vyshinskii, I.M., Realization of
Variability in Silk Worm, Problemy genetiki i teorii
evolyutsii (Problems of Genetics and Evolution Theory),
Novosibirsk: Nauka, pp. 99–114.
43. Astaurov, B.L., Investigation of Hereditary Change in
Halteres of Drosorhila melanogaster Shin, Zh. Eksper.
Biol., Ser. A., 1927, vol. 3, nos. 1–2, pp. 1–61.
44. Dragavtsev, V.A., K probleme geneticheskogo analiza poli-
gennykh kolichestvennykh priznakov rastenii (Genetic
Analysis of Polygenic Quantitative Traits in Plants), St.
Petersburg: VIR, 2003.
45. Dragavtsev, V.A., On the Gap between Plant Genetics
and Plant Breeding and the Ways to Overcome It, Vestn.
Saratovskogo Gosagrouniversiteta im.Vavilova, 2004,
no. 1, pp. 10–15.
RUSSIAN JOURNAL OF GENETICS Vol. 42 No. 9
1065
46. Morgan, T.G., Razvitie i nasledstvennost’ (Development
and Heredity), Leningrad: Biomedgiz, 1937.
47. Goldschmidt, R., Physiologische Theorie der Ver-
erbung, Berlin: Springer, 1927.
48. Mayr, E., Animal Species and Evolution, Cambridge:
Harvard Univ. Press, 1963.
49. Waddington, C.H., Organisers and Genes, 1940.
50. Waddington, C.H., New Patterns in Genetics and Devel-
opment, New York: Columbia Univ. Press, 1962.
51. Waddington, C.H., Towards a Theoretical Biology: Pro-
legomena, Birmingham: Aldine, 1968.
52. Churaev, R.N., A Hypothesis on Epigene, Issledovaniya
po matematicheskoi genetike (Studies in Mathematical
Genetics), Novosibirsk: Inst. Tsitol. Genet. SO RAN,
1975, pp. 77–94.
53. Churaev, R.N., Elementy nekanonicheskoi teorii nasled-
stvennosti (Elements of Noncanonical Heredity), Ufa:
Ufimskii Nauchn. Tsentr, 1977.
54. Churaev, R.N., Stupak, I.V., Tropynina, T.S., and Stu-
pak, E.E., Construction of a Two-Component Epigene
with Preset Characteristics, Dokl. Ross. Acad. Nauk,
2001, vol. 378, no. 6, pp. 837–840.
55. Takhtadzhan, A., Principia tectologica. Printsipy orga-
nizatsii i transformatsii slozhnykh sistem: evolyutsionnyi
podkhod (Principia tectologica. Principles of Organiza-
tion and Transformation of Complex Systems: An Evo-
lutionary Approach), St. Petersburg: SPKhFA, 2001.
56. Chadov, B.F., Facultative Dominant Lethals: Genetics,
Ontogeny, and Phylogeny, Evolyutsionnaya biologiya
(Evolutionary Biology), Stegnii, V.N., Ed., Tomsk:
Tomsk. Gos. Univ., 2002, vol. 2, pp. 118–142.
57. Chadov, B.F., Species Transformation and Speciation:
Two Forms of Evolutionary Transformation of Living
Organisms, Evolyutsiya zhizni na Zemle (Evolution of
Life on the Earth), Podobina, V.M., Ed., Tomsk: Tomsk.
Gos. Univ., 2005, vol. 3.
58. Nicolis, G. and Prigogine, I., Self-Organization in Non-
Equilibrium Systems, New York: Wiley–Interscience,
1977.
59. Haken, H., Synergetics, Heidelberg: Springer, 1978.
2006