Introduction

– Hormone is a molecule that is secreted into the extracellular fluid, circulates in

the blood or heamolymph and communicates regulatory message throughout the
body.
– Endocrine gland is made up of ductless glands that release hormone into the
bloodstream.
– Exocrine gland has duct that carry secreted substances onto body surface or into
body cavities.

Comparison between endocrine system and nervous system

Endocrine system Feature Nervous system

Transmitted in the form of
chemical substance
By the circulatory system
Slow
Long-lasting
Carried by blood to
targeted cell
Many different
Graded response
Nature of information
Mode of transmission
Speed of transmission
Duration of effect
Localization of effect
Nature of chemical
coordination
Nature of response
Transmitted in the form of
electrical impulse
By the nervous system
Rapid
Short-lived
Transmitted by nerve fibre
to particular destination
Only a few types
Follows all-or-none law

There are two types of hormones

1. Water-soluble hormone (peptide and amino-based hormone)

– ADH
– Insulin
– FSH
– LH

1. Lipid-soluble hormone (steroid hormone)

– Progesterone
– Oestrogen
– Testosterone
Mechanism of action via gene activation

1. Some hormones such as steroid hormones are lipid-soluble so they can enter
easily through the phospholipid layer of the cell.
2. In the cytoplasm, the hormone binds to its receptor to form a hormone-receptor
complex.
3. The hormone-receptor complex then enters nucleoplasm and binds to a specific
section of DNA which functions as a gene.
4. The complex stimulates the gene to transcribe messenger RNA (mRNA).
5. The mRNA moves to the cytoplasm and directs the synthesis of proteins that alter
the activity of the cell.
Mechanism of action via cAMP (signal transduction mechanism)

1. Peptide and amino-based hormone serves as the first messenger binds to the
receptor (G protein-coupled receptor) in the plasma membrane and forms
hormone-receptor complex.
2. The hormone-receptor complex binds to and activates G-protein in the membrane.
3. The activated G-protein then binds to the enzyme adenylyl cyclase and activates
it.
4. The activated adenylyl cyclase catalyses the conversion of ATP to cAMP.
5. cAMP acts as the second messenger which initiates a complex chain reaction.
6. cAMP activates the inactive enzyme protein kinase which in turn activates
inactive enzyme phosphorylase kinase.
7. Active phosphorylase kinase then activates the inactive enzyme glycogen
phosphorylase that catalyses the breakedown of glycogen to glucose phosphate.
8. This results in a cascade where the action of an enzyme in turn activates another
enzymatic reaction producing many product molecules. This brings about an
amplified and rapid response to the non-steroid hormone.
Menstrual cycle

1. The cycle begins with the release from the hypothalamus of GnRH
2. Which stimulates the anterior pituitary gland to secrete small amounts of FSH and
LH.
Follicular phase
3. FSH stimulate follicle growth, aided by LH
4. The cell of growing follicle starts to make oestrogen. The low level of oestrogen
inhibits secretion of the pituitary hormones, keeping the levels of FSH and LH
relatively low.
5. When oestrogen secretion by the growing follicle begins to rise steeply,
6. The FSH and LH levels increase markedly. Whereas a low level of oestrogen
inhibits the secretion of pituitary gonadotrophins, a high concentration has the
opposite effect. It stimulates gonadotrophins secretion by acting on the
hypothalamus to increase its output of GnRH. The effect is greater for LH
because high concentration of oestrogen increases the GnRH sensitivity to LH-
releasing cell in the pituitary gland. In addition, follicle responds more strongly to
LH at this stage because more of their cells have receptor for LH. The increase in
LH concentration by increased oestrogen secretion from the growing follicle is an
example of positive feedback. The result is final maturation of the follicle.
Ovulation
7. The maturing follicle, which contains an internal fluid-filled cavity, grows very
large, forming a bulge near the surface of the ovary. The follicular phase ends at
ovulation, about a day after the LH surge. In response to the peak in LH levels,
the follicle and adjacent wall of the ovary rupture, releasing secondary oocyte.
Luteal phase
8. LH stimulates the follicular tissue left behind the ovary to transform into the
corpus luteum. Under continued stimulation of LH, the corpus luteum secretes
oestrogen and progesterone. As the oestrogen and progesterone levels rise, the
combination of these hormones exerts a negative feedback to the hypothalamus
and pituitary, reducing the secretion of LH and FSH to very low levels.
Menstruation
Near the end of the luteal phase, low gonadotrophins levels cause the corpus
luteum to disintegrate, triggering a sharp decrease in oestrogen and progesterone
concentration. The decreasing levels of ovarian steroid hormones liberate the
hypothalamus and pituitary gland from the negative-feedback effect of these
hormones. The new cycle begins with the secretion of FSH and LH by pituitary
gland.
Role of hormones during pregnancy

– When fertilized egg is anchored in the endometrium, HCG hormone is produced

to replace the role of LH to maintain the secretion of oestrogen and progesterone
in the first trimester.
– HCG hormone drops and corpus luteum degenerates. The role of corpus luteum is
taken over by placenta in the second trimester.
– Combination of oestrogen and progesterone
Maintain the development of endometrium and thus prevent menstruation
Inhibit the release of FSH
Inhibit the release of prolactin
– Oestrogen
Stimulate the development of mammary glands for lactation
Increase the size of myometrium
Trigger the formation of receptor to hormone oxytocin in the uterine muscle
– Progesterone
Inhibit contraction of myometrium
Stimulate the development of mammary glands for lactation
– Towards the end of pregnancy (third trimester), the level of progesterone decrease
and trigger onset of parturition.
The decrease of progesterone levels causes the contraction of myometrium.
Oestrogen increases the sensitivity of myometrium to oxytocin.
The contraction of myometrium some more stimulates the posterior pituitary
gland to secrete more oxytocin.
At the same time, it stimulates the placenta to produce prostaglandins to increase
the power of myometrium contraction.
– After the birth, the progesterone and oestrogen concentration decline sharply due
to the loss of placenta.
– Prolaction is no longer inhibited and is released to stimulate mammary glands to
produce milk.
– Oxytocin stimulates the release of milk from mammary glands.
Lactation

– Lactation is the production of milk for nourishing the young.

– After birth, prolactin is secreted by the anterior pituitary gland to stimulate milk
production.
– When baby suckle, the posterior pituitary secretes oxytocin to eject milk from the
alveoli into the duct.
 – Breastfeeding promotes recovery of the uterus because oxytocin released during
breastfeeding stimulates the uterus to contract to normal size.

Plant hormone

Auxin

1. Role in cell elongation

– Low concentration of auxin may stimulate cell elongation in the apical meristem
but higher concentration may inhibit cell elongation by inducing production of
ethylene, hormone that inhibits cell elongation.
– Acid growth hypothesis – auxin stimulate plasma membrane to pump H ions into
cell wall and lowers its pH. Acidification of cell wall activates expansions that
break the cross-link between cellulose myofibrils. Lower water potential triggers
intake of water and increases the turgor pressure and in turn increase cell wall
plasticity which causes cell to elongate.
– Stimulate the sustained growth response (addition of cytoplasm and wall material)
for cell elongation.
1. Lateral and adventitious root formation
– Auxin involves in branching of root.
 – Treating detached leaf or stem with rooting powder containing auxin cause
adventitious root to form.
1. As herbicide
– Monocot can rapidly inactivate auxin as herbicide.
– Eudicots cannot and therefore die from hormonal overdose.
1. Other effect
– Auxin affects secondary growth by increasing cambial activity and influencing
differentiation of cambial initials.
– Promote fruit growth.
– Induce fruit development without pollination.

Cytokinins

1. Control of cell division and differentiation

– Work with auxin at certain ratio to stimulate cell differentiation.
– Increase cytokinins levels, shoot buds develop.
– Increase auxin levels, roots form.
1. Control of apical dominance
– Auxin and cytokinins act antagonistically in regularing axillary bud growth.
– Auxin inhibits axillary bud growth.
– Cytokinins counter the action of auxin by signaling axillary bud to begin growing.
1. Anti-aging effects
– Cytokinins slow down the deterioration of cell by inhibiting protein breakdown,
stimulating RNA and protein synthesis and mobilizing nutrients from surrounding
tissues.

Gibberellins

1. Stem elongation
– Stimulate stem and leaves growth but have little effect on foots.
– In stem, it stimulates cell elongation and cell division.
– Act in concert with auxin to promote cell elongation.
1. Fruit growth
– Auxin and gibberellins must be present in order for fruit to develop.
1. Germination
– Gibberellins signal the seed to break dormancy and germinate.

Abscisic acid

1. Seed dormancy
– Inhibits seed dormancy during seed maturation and induce the production of
certain proteins that helps the seed withstand dehydration.
 1. Drought tolerance
– Accumulate in leaves and causes stomata to close rapidly.
– Cause potassium channel of the guard cell to open, leading to a massive loss of
calcium ion and is followed by osmotic pressure.

Ethylene

1. The triple response to mechanical stress

– Enable the young shoot to avoid the obstacle when growing up from the soil.
– Triple response = slowing of stem elongation, thickening of the stem, curvature
that cause the stem to grow horizontally.
– Whenever there is obstacle, ethylene is produced to inhibit vertical elongation.
– Production of ethylene decreases when no obstacle is detected, vertical elongation
is resumed.
1. Senescence
– A burst of ethylene is almost always associated with the programmed destruction
of cells, organs or the whole plant during autumn.
1. Leaf abscission
– A change in the ratio of ethylene to auxin controls abscission.
– Aging leaf produces less auxin, rendering the cells of abscission layer more
sensitive to ethylene.
1. Fruit ripening
– A burst in ethylene production in fruit triggers the ripening process.
– Stimulate the enzymatic breakdown of cell wall components to soften the fruit
and conversion of starch to sugar to make fruit sweet.
– The production of new scents and colours helps advertise ripeness to animals.

Phytochrome

1. Plants have a light-detecting system known as phytochrome which plays a role in

plants development, seed germination as well as flowering.
1. A phytochrome has two identical subunits, each consisting of a polypeptide
component covalently bonded to a non polypeptide chromophore, the light-
absorbing part of the subunit.
2. The chromophore of a phytochrome is photoreversible, reverting back and
forth between two isomer forms, depending on the colour of light.

3. In its Pr isomer form, a phytochrome absorbs red light maximally, whereas in

its Pfr isomer form, it absorbs far-red light.
4. Pfr triggers mamny of a plant’s development responses to light.
5. Conversion to Pfr is faster than the conversion to Pr. therefore the ratio of Pfr to
Pr increase in sunlight.
Photoperiodism

1. Photoperiod is the relative lengths of daylight and darkness that a plant is exposed
in a 24-hour cycle.
2. Photoperiodism is the physiological response to photoperiod, such as flowering.

Short-day plant

– Plants that require a light period shorter than a critical length to flower.
– Example: chrysanthemums, poinsettias and some soybean.

Long-day plant

– Plants that require light period longer than a certain number of hours to flower
– Example: spinach, radishes, lettuce, irises and many cereal varieties.

Day- neutral plant

– Plants that are not affected by photoperiod and flower regardless of day length.

1. The photoreceptor of photoperiodism is phytochrome. The balance between two

isomers of chromophore, controls the flowering in short-day and long-day plant.
2. Pfr stimulates flowering of long-day plants but inhibits flowering in short-day
plants.
3. Florigen, a chemical messenger that transmits information from leaves to flower
buds, is secreted in response to relative amounts of two forms of phytochrome.
4. There are two inactive forms of florigen: one of which is converted to florigen in
the absence of Pfr, the other in the presence of Pfr.
5. In long-day plants, the inactive hormone is activated by the presence of Pfr while
in short-day plants, the inactive hormone is activated by the absence of Pfr.
1. When the dark period is shorter than a critical dark period, the long-day plants
will flower but short-day plants will not flower.
2. When the dark period is longer than a critical dark period, the long-day plants
will not flower but short-day plants will flower.
3. A flash of red light interrupting the dark period shortens the dark period.
Hence, there is flowering in long-day plants but not short-day plants.
4. A subsequent flash red light followed by far-red light cancels the effect of red
light. Hence, there is flowering in short-day plants but not long-day plants.
5. If a red light flash followed by a flash of far-red light, and then red light flash
again, there is flowering long-day plants but not short-day plants.
6. Therefore, it can be concluded that the flowering of long-day plants or short-
day plants is determined by the last flash of light which favours the either
plants.