Lecture 12: Metamorphosis

A rapid transformation in an animal's body structure from one developmental stage to a completely different one, typically from immature to adult.

A post-embryonic process where a larval or immature stage undergoes a significant transformation into the adult stage.

The fertilized egg develops into an embryo, which eventually hatches into a tadpole.

The initial stage after hatching, characterized by external gills, a developing mouth, and an aquatic lifestyle.

The process of programmed cell death that eliminates larval structures like gills and tails.

The development of new structures, like limbs and lungs, for terrestrial life.

The transformation of larval organs, such as the intestines, into their adult forms.

Environmental cues like temperature, light, and photoperiod trigger metamorphosis in amphibians.

The hypothalamus in the brain detects environmental cues and releases CRH (corticotropin-releasing hormone).

CRH stimulates the pituitary gland to release TSH (thyroid-stimulating hormone), which is crucial for metamorphosis.

TSH travels through the bloodstream to the thyroid gland and stimulates the production of thyroid hormones.

T3 (triiodothyronine) and T4 (thyroxine), collectively called T8, are the key thyroid hormones driving metamorphosis.

T3 and T4 drive the transformation of tadpoles into frogs, including the development of limbs and lungs.

Thyroid hormones provide feedback to the hypothalamus, ensuring sustained production and promoting continuous metamorphosis.

The conversion of T4 to T3 is facilitated by the enzyme diodinase, which removes one iodine group from T4.

T3 is the active form of the thyroid hormone, while T4 acts as a prohormone.

The initial phase of metamorphosis where the thyroid gland is small and thyroid hormone levels are low. This stage prepares the organism for the upcoming changes.

A gradual increase in thyroid hormone levels during metamorphosis, leading to initial changes in the organism. This phase involves the development of limb buds and increased activity of the thyroid gland.

The peak phase of metamorphosis, marked by the highest thyroid hormone levels and rapid changes in the organism's body structure. Limb development is complete, and internal changes like gill resorption and organ remodeling take place.

The final phase following the climax, where thyroid hormone levels drop to the lowest point. This signifies the completion of metamorphosis and the transition to adulthood.

The process of actively absorbing and utilizing radioactive iodine by the thyroid gland. The amount of uptake can be used to assess the gland's activity and size.

The process of developing limb buds, which are the initial structures that will eventually evolve into limbs during metamorphosis.

The gradual increase in thyroid hormone levels during pro-metamorphosis, which triggers many changes in the organism's body.

The progressive development of the thyroid gland during metamorphosis, indicating an increase in its activity.

The restructuring and remodeling of the organism's internal organs, including those like the intestines, during metamorphosis. This process prepares the organs for their new functions in the adult stage.

Thyroid hormone (TH) regulates the development of all cell types involved in limb formation during amphibian metamorphosis, including nerves, cartilage, and muscle.

A dominant negative thyroid receptor (DNTR) acts within the cell where it is expressed, blocking TH signaling specifically in that cell type.

By expressing DNTR in specific cell types, scientists can block TH signaling only in those cells, allowing them to study how TH directly impacts different cell types during limb development.

TH directly influences the development of muscle cells during limb formation. When TH signaling is disrupted in muscle cells, muscles fail to develop.

The thyroid receptor (TR) binds to thyroid hormone (TH) to activate genes involved in metamorphosis.

Thyroid receptor (TR) is a protein that acts as a switch for genes involved in metamorphosis. It determines whether a gene is turned on or off.

Dominant negative TR (DNTR) binds to DNA but cannot activate it, effectively blocking any activity of the thyroid hormone.

The DNTR binds to DNA but cannot activate it, preventing the transcription of genes important for metamorphosis. This leads to the inability of frogs to undergo metamorphosis.

In metamorphosis, thyroid hormone (TH) directly induces apoptosis in some intestinal epithelial cells, causing their programmed death.

T3, the active thyroid hormone, indirectly induces apoptosis in epithelial cells by activating fibroblasts in the connective tissue to send signals to the epithelial cells.

Thyroid hormone (TH) promotes tissue remodeling during metamorphosis, including the transformation of the intestine into its adult form.

In the experiment with wild type tadpoles, the presence of thyroid hormone (T3) leads to tail regression and the production of collagenase, which breaks down the tail.

The dominant-negative (DNTR) mutation prevents tadpoles from undergoing metamorphosis even when given T3 or thyroxine.

Dominant negative transgenic tadpoles cannot undergo metamorphosis even with the presence of T3, causing them to grow larger but retain their tails.