Eukaryotic Gene Expression Can Be Regulated by Intercellular and Intracellular Signals

The effects of steroid hormones (and of thyroid and retinoid hormones, which have the same mode of action) provide additional well-studied examples of the modulation of eukaryotic regulatory proteins by direct interaction with molecular signals (see Fig. 12-40). Unlike other types of hormones, steroid hormones do not have to bind to plasma membrane receptors. Instead, they can interact with intracellular receptors that are themselves transcriptional transactivators. Steroid hormones too hydrophobic to dissolve readily in the blood (estrogen, progesterone, and cortisol, for example) travel on specific carrier proteins from their point of release to their target tissues. In the target tissue, the hormone passes through the plasma membrane by simple diffusion and binds to its specific receptor protein in the nucleus. The hormone-receptor complex acts by binding to highly specific DNA sequences called hormone response elements (HREs), thereby altering gene expression. Hormone binding triggers changes in the conformation of the receptor proteins so that they become capable of interacting with additional transcription factors. The bound hormone-receptor complex can either enhance or suppress the expression of adjacent genes.

The DNA sequences (HREs) to which hormone-receptor complexes bind are similar in length and arrangement, but differ in sequence, for the various steroid hormones. Each receptor has a consensus HRE sequence (Table 28-4) to which the hormone-receptor complex binds well, with each consensus consisting of two six-nucleotide sequences, either contiguous or separated by three nucleotides, in tandem or in a palindromic arrangement. The hormone receptors have a highly conserved DNA-binding domain with two zinc fingers

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Essentials of Human Physiology

Essentials of Human Physiology

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