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We are All-in-One and One-in-AII

Sun, 05/30/2010 - 15:34 — makhp

In 1826, the german biologist, Ernst Haeckel, noticed something strange when he was studying the
embryonic developmental stages of vertebrates. At some stage in their embryonic development, they all
looked more or less the same. So he came up with a hypothesis, called the biogenetic law, that states that
advanced organisms undergo the developmental stages of their previous species before they matured. This
was shortformed to a scientific explanation: Ontogeny ( the study of embryonic development) recapitulates
Phylogeny ( t h e evolutionary stages of the organism). This theory is also called "the Recapitulation Theory"
because of this.

We can see Haeckel's drawing to the left here. Taking

ourselves as examples, this would mean that we went
through becoming first a fish, then an amphibian, then a
reptile before becoming a human being while we were in
our mother's womb. Although most vertebrates have
some history where their embryos formed "primitive"
organs, ( we had gill slits when we were embryos, but
these did not fully develop into gills, and all of them
closed, except for one, which became our ear canal.
Dolphins, whales and snakes also had "primitive legs"
when they were embryos, but again, these did not form
or function fully when they were adults.) These organs
or appendages never fully functioned and were
discarded or reabsorbed by the embryo. Although not
accepted now (i.e. proven to be "scientifically untrue"),
the theory did generate in most biologists' minds a perpetual question: "Do we all really share something in
common?" By "all" is meant not only vertebrates but invertebrates or all animals in general.

The theory was laid to rest, until bithorax and Antennapedia came along. These are two mutants in
Drosophila that was discovered in 1995 by Edward B Lewis. It showed that development in the fruitfly
Drosophila depended o n a s e t o f g e n e s t h a t controlled the orientation of the anterior and posterior position
of the body, as well as the expression of certain genes along its length. ( Albeit, many other factors
influence what a cell will eventually become in our body, such as the concentration gradient of substances
(especially retionic acid in embryos), the location of the cell and interactions between the cell and its
neighbouring cells - but the effect of this gene set is also of major importance in determining embryonic
development.

:
something went wrong, e.g. if the third segment of this fly (which normally had
ery small wings called halteres to balance the fly during flight) failed to be defined
ut instead copied the orders from the genes in the second segment, we get a fly with
>ur wings.

Similarly, if the antenna of the fly gets mixed up with genes ordering for the
formation of legs, we get legs comming out where the antennas should be. (as in
antennapedia ). Lewis showed that these set of genes are very important for the
formation of the fly body. ( He was awarded the Nobel prize for medicine for that
year for this work.)
 So they "redrew" Haeckel's diagram and the "modern" version
would be something like this on the left. The study of hox genes
was a start in the direction of a new study in biology, called
"Evolutionary Development" or Evo Devo for short. Started
around 10 years ago, this branch of biology is slowly gaining
importance due to its significance of finding common ground
among the scientists who are working to understand how
genetic development can influence embryonic development.
Among the achievements of evo devo are the following:

1. The tinman gene in Drosophila, which affects heart

development, was also found in mouse and man as the Csx
gene, and this study has helped the development of medication
and therapy for this heart ailment by offering the fruitfly and
mouse as alternatives for gene technology and drug
therapeutics for the disease.

2. The patched gene in mouse which, if absent in one of the two

copies found in natural mice, causes brain tumors and basal
(skin) cell carcinomas, was found to be the same gene in man
which causes Basal Cell Nervus Syndrome- or BCNS, a skin

Comments

Something in common among Plants sun, 05/30/2010 - 23:30 - makhp

As in animals, so in plants:

Plants, too, share a common set of genes (these are called MADS genes - because they were isolated as 4
genes identical to MCM1 (found in yeast), Agamous (from the plant Arabidopsis), Deficiens (from
snapdragon) and SRF (from man)) that control their development, but this time, more in floral development
of whorls (concentric rings) of floral structures. A basic structure of an angiosperm flower will show 4
whorls, as below:

There are 4 whorls in a flower: Sepals (Se), Petals (Pe),

Stamens (St) and Carpel (Ca), from outside to inside. The MADS
genes that control this model have been studied extensively in a
 plant called the thale cress ( Arabidopsis th aliana ) which looks
like this:

ft model used to explain MADS action on

the flower of Arabidopsis was explained
beautifully by Professor P Z Meyers in the
Pharyngula website. He used a model
which he called an ABC model which is
shown below:

In this model, three genes ( A, B and C) control the formation of

structures around the flower. The control is not a simple
one-to-one relationship, however. Rather than to re-explain
what the great proffessor has explained ( which I am sure I
cannot do him justice), I would attempt to use an interaction
matrix ( in the form of a "punnet square" model which Form 6
Biology students have seen a lot of during their studies in
genetics) to define the functions of A, B and C.

Reading from left to right, A

(by itself) turns on the
genes for Sepal formation.
Interacting with B, they
turn on the gene for Petal
formation. A also
suppresses C.

(by itself), turns on

irpel formation.
Interacting with B, they turn on Stamen formation. C also suppresses A. B is an interacting gene. B by itself
does nothing.

Using this model, the following mutants in Arabidopsis can be explained.

Apetala2 mutant: This mutant developed only

:arpel and stamens, but not petals or sepals.

\petala3 mutant: This mutant developed only

:arpels and sepals, but not petals or stamens.

\gamous mutant: This mutant developed only

petals and sepals, but not carpels or stamens,
rhese photos from Pharyngula website shows
these mutants and the genes that are active
 ro obtain the Apetala2 mutant, simply delete A gene effects, and we are
left with only S t a n d Ca as results, (i.e. Apetala2 is the mutant condition
where mutation resulted in a defective MADS A gene.)

Similarly, removing B results in only Sepals and Carpel being formed.

This is the Apetala3 mutant.

Finally, to get agamous mutant, we delete C gene.

So you can see here that mutations actually teach us a lot about the
interaction and role of genes in the development of structures.

There are HOX genes in plants too, and there are MADS genes in
animals. But although they share these genes, in plants HOX plays a
role other than controlling orientation, whereas in animals, MADS
probably plays a role other than whorl control. Biologists are still
studying this aspect, but definitely, it is clear that there are some
DNA sequences that remain unchanged by evolution and are carried
down in plants and animals.

The question "Do we really share something in common" is really (to me) a further expansion of the
question "What makes us human?" and it has taken us through such a journey we trully never would have
imagined.

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