PMID:16675526

Citation	Lai, GJ and McCobb, DP (2006) Regulation of alternative splicing of Slo K+ channels in adrenal and pituitary during the stress-hyporesponsive period of rat development. Endocrinology 147:3961-7
Abstract	Stress triggers release of ACTH from the pituitary, glucocorticoids from the adrenal cortex, and epinephrine from the adrenal medulla. Although functions differ, these hormone systems interact in many ways. Previous evidence indicates that pituitary and steroid hormones regulate alternative splicing of the Slo gene at the stress axis-regulated exon (STREX), with functional implications for the calcium-activated K+ channels prominent in adrenal medullary and pituitary cells. Here we examine the role of corticosterone in Slo splicing regulation in pituitary and adrenal tissues during the stress-hyporesponsive period of early rat postnatal life. The sharp drop in plasma corticosterone (CORT) that defines this period offers a unique opportunity to test CORT's role in Slo splicing. We report that in both adrenal and pituitary tissues, the percentage of Slo transcripts having STREX declines and recovers in parallel with CORT. Moreover, addition of 500 nm CORT to cultures of anterior pituitary cells from 13-, 21-, and 30-d postnatal animals increased the percentage of Slo transcripts with STREX, whereas 20 microm CORT reduced STREX representation. Applied to adrenal chromaffin cells, 20 microm CORT decreased STREX inclusion, whereas neither 500 nm nor 2 microm had any effect. The mineralocorticoid receptor antagonist RU28318 abolished the effect of 500 nm CORT on splicing in pituitary cells, whereas the glucocorticoid receptor antagonist RU38486 blocked the effect of 20 microm CORT on adrenal chromaffin cells. These results support the hypothesis that the abrupt, transient drop in CORT during the stress-hyporesponsive period drives the transient decline in STREX splice variant representation in pituitary, but not adrenal.
Links	PubMed Online version:10.1210/en.2005-1551
Keywords	Adrenal Medulla/cytology; Adrenal Medulla/growth & development; Adrenal Medulla/physiology; Alternative Splicing/physiology; Animals; Cells, Cultured; Chromaffin Cells/cytology; Chromaffin Cells/physiology; Corticosterone/blood; Gene Expression Regulation, Developmental; Hydrocortisone/blood; Hypophysectomy; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/chemistry; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/genetics; Large-Conductance Calcium-Activated Potassium Channels/chemistry; Large-Conductance Calcium-Activated Potassium Channels/genetics; Male; Pituitary Gland, Anterior/cytology; Pituitary Gland, Anterior/growth & development; Pituitary Gland, Anterior/physiology; Protein Structure, Tertiary; Rats; Rats, Sprague-Dawley; Receptors, Glucocorticoid/metabolism; Receptors, Mineralocorticoid/metabolism; Stress, Physiological/genetics; Stress, Physiological/physiopathology; Testis/physiology; Testosterone/blood
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
RAT:KCMA1	involved_in	GO:0031960: response to corticosteroid	ECO:0000314: direct assay evidence used in manual assertion		P		Seeded From UniProt	complete

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