14.          METAMORPHOSIS

The term metamorphosis is derived from two Greek words i.e. meta- “change” and morphe -“form”. Thus defined as Metamorphosis is a biological process of profound physical changes through cell division and differentiation that occur in some non-mammalian animal species during development from larval to the adult form. The metamorphosis is accompanied by the change in habitat or behaviour and it is a characteristic feature of some insects, fishes, amphibians, molluscs, cnidarians, crustaceans, tunicates and echinoderms. The developmental processes are reactivated by specific stimuli during metamorphosis, by which the whole body of an organism is re-differentiated to prepare for a new mode of existence.

14.1.      Amphibian Metamorphosis

During amphibian metamorphosis, many morphogenetic changes occur that enables the existence of a new form of the transformed individual, which are listed below.

The process of amphibian metamorphosis is regulated by Thyroxin (T3&T4) hormone from thyroid and their counteracting prolactin hormone. T3 is considered as more critical for metamorphic changes because it can induce the changes at low concentration than T4.

The changes made by T3 /T4 are specific.  T3 /T4 causes differentiation of tissue and some tissues undergo degeneration. The morphogenetic and biochemical changes occur during an amphibian (anuran) metamorphosis are listed below.

During tail degeneration, the cells of epidermal, notochordal and neural tissues go to apoptosis and are disintegrated by their own digestive enzymes like collagenase and metalloprotease. These enzymes are synthesised by thyroxines. The most regional specific changes brought by T3 is epidermal differentiation into a new set of glands on head and body of Tadpole. T3 also causes apoptosis of the tail epidermal cells and a tail-specific suppression of stem cell divisions in the same tadpole.

The amphibian metamorphosis is also influenced by the photoperiodicity and circadian rhythms, i.e. the tadpoles kept in dark places shows a slow rate of metamorphosis, caused by melatonin. Melatonin is a pineal secretion. The hormonal responses from regional epidermis which appears to be controlled by the dermal mesoderm and does not alter even after changing the ectoderm by transplantation.

14.2.      Experiment

If a tail tip is transplanted to the trunk region or eyecup is placed in the tail region. The transplanted tail tip is not protected from degeneration, but the eyecup placed in degenerative tail region retains its integrity. The threshold concept model about the coordination of developmental steps during metamorphosis and the related experiments reveals that the timing of metamorphosis appears to be regulated by the sensitivity of different tissues to thyroid hormones. For example, when thyroid hormone levels gradually rise, the hind limbs develop first and then the tail degenerates.

The thyroid hormone acts as a transcription factor by activating or repressing many genes. First of all, they activate the expression of two major types of thyroid hormone receptors (TR), i.e. TR α and TR β.

The thyroid hormone receptor binds specifically to the chromatin even prior to thyroid hormones and thought to be a transcriptional repressor but after binding with T3 & T4, the hormone-receptor complex becomes a strong transcriptional activator for genes. Many genes are expressed by T3/T4 like albumin, carbamoylphosphate synthase, adult globins, adult skin keratin, homologue of sonic hedgehog and it also raises the thyroid hormone receptor synthesis dramatically. Such autoinduction of thyroid hormone receptor by T3 significantly enhances the rate of metamorphosis.

The increasing amount of T3 receptors in a tissue make it competent to respond to T3 hormones and the visible changes of metamorphosis occur rapidly. This further leads to enhanced production and induction of more T3 receptors. The time at which such induction occurs is known as the metamorphic climax.

The thyroid hormone receptor forms a dimer with the retinoid receptor (RXR) that binds thyroid hormones and enter the nucleus to affect the transcription.

14.3.      Heterochrony

The term derived from the Greek words, “hetero-other" and “Chronos -time". It refers to the rate of morphological transformations accomplish by the developmental timing of events over evolutionary time leading to changes in size and shape. It is related to the animals showing allometric growth instead of isometric. During allometric growth, the development rate of body organs of an organism is not similar. There are three major types of Heterochrony are seen among animal species that are

Neoteny: Germ line cell development proceeds at the same rate as in an ancestral species, but somatic cell development is delayed as compared to the rate in their ancestor. Thus the larva looks like an adult.

Pedogenesis: Somatic development proceeds at the same rate as in an ancestral species, but germline cell development rate is enhanced as compared to the rate in their ancestor. Thus organism starts reproduction in the larval stage.

Direct development: The type of Heterochrony in which the embryo avoids the intermediate stages of development and develops directly as the miniature of the adult.

14.4.      Insect Metamorphosis

Insect metamorphosis involves the degeneration of larval tissues and their complete replacement by different cell population. Usually, insects grow by moulting, shedding their cuticle and developing new cuticle as their size increases. The three major patterns of insect development.

Ametabolous development: 

In this type of development, the insects hatch the egg as a pronymph that resembles the adult characters and grow directly as an adult without an intermediate stage. e. g.  springtails and mayflies.

Hemimetabolous development: 

The development of insect includes the hatching from pronymph as the immature adult, nymph. The nymph develops gradually with each moult and finally become an adult. e.g. bugs and grasshopper.

Holometabolous development: 

The insect hatches in a juvenile form, the larva that grows in size with each moult. Then the larvas shows metamorphose is to pupa, the stage of transformation. Then finally adult shows a resemblance from the pupa. e.g. beetles, moths and butterflies.

The larva composed of two distinct populations of cells: the larval cells- for juvenile insect, and the cluster of imaginal cells awaiting the signal to differentiate.

Hormonal control of insect metamorphosis

The moulting process is initiated by the release of a peptide family, prothoracicotropic hormone (PTTH) in response to neural, hormonal, or environmental factors, to stimulate the production of ecdysone from the prothoracic gland. Ecdysone is a prohormone converted into 20-hydroxyecdysone, an active form by a heme-containing oxidase in the mitochondria and microsomes of peripheral tissues. Each moulting organized by the surge of 20-hydroxyecdysone that commits and stimulates the epidermal cells to synthesize enzymes for digestion and recycling of the cuticle components.

Environmental conditions may also control moulting for example in silkworm moth the PTTH secretion ceases after the pupa formation and the development suspended throughout the winter season at a state, called diapause. If the pupa not exposed to cold weather the diapause lasts for a very long time but if exposed to cold for even two weeks, then pupa can moult when returned to a warmer temperature.

The juvenile hormone (JH) is the second major hormone in insect development secreted from corpora allata. It prevents metamorphosis during larval moults. In the presence of juvenile hormone, the hydroxyecdysone-stimulated moults lead to a new larval instar. As juvenile hormone levels drop below a critical threshold value it triggers the secretion of prothoracicotropic hormone from the brain that stimulates the prothoracic glands to secrete a small amount of ecdysone.

Then the hydroxyecdysone formed in the absence of juvenile hormone commits the cells to pupal development through which new mRNAs are synthesized and translated to inhibit the transcription of the larval mRNAs. The second ecdysone surge activates the expression of new pupal genes to transform the larva to pupa.

As shown in the curves of the above Figure, the different cells show responses to the JH at different times. The onset and duration of the JH-sensitive time period is an autonomous state of the cell that is not controlled by hormones. The critical weight during the last larval stage acts as a checkpoint to initiates metamorphosis through an endocrine cascade. When the insect's body has stored all the food it needs to undergo these major changes and no needs to feed. If the diet is poor then the larval period is extended to ensure the critical weight but if corpora allata is removed from larvae in their last instar then they don’t show any adjustment to starvation. Thus, the continuing presence of the juvenile hormone in the last instar can delay the initiation of metamorphosis and the removal of only juvenile hormone (JH) can’t allow the larva to enter metamorphosis. Means there is not only an optimum weight but also a minimum time that is required to initiating metamorphosis.

Next Previous