Molecular response to thyroid hormones, Operation Management

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Molecular Response to Thyroid Hormones during Metamorphosis

Thyroid hormones can cause obtainable tissues to break down or can remold the tissues to their adult function. The liver cells of the tadpole for instance are not destroyed and replaced during metamorphosis. In place of their structure is remodeled. This change is accompanied by dramatic raise in ribosomal and messenger RNA synthesis. The rate of protein synthesis also increases nearly 100 folds in four hours of thyroid hormone stimulation. Many of the new mRNAs are those that code for new functions of the liver. The main increase in protein synthesis appears to come from the transcription of new m-RNAs.

Carbamoylphosphate synthase (a urea cycle enzyme) is synthesized after the burst of RNA synthesis. Experiments have illustrated three types of molecular response to thyroid hormone. One set of genes increases its low level of transcription in reply to either natural or thyroxine induced metamorphosis. Another set of genes decreases its rate of transcription, whereas a third set of genes remains unaffected by thyroid hormones. Mori and Coworkers (1979) have illustrated that much of the increase in Carbamoylphosphate synthase can be attributed to increased transcription from the gene. So metamorphosis appears to some extent to be controlled at the transcriptional level. Other evidences also indicate the capability of thyroid glands to regulate gene activity at the level of transcription. This does not mean that transcription is the only level of gene regulation, operative during metamorphosis, but it is obviously an important one.


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