Developmentally regulated polyadenylation of two discrete messenger ribonucleic acids for mullerian inhibiting substance
Department of Pediatrics
Medical Subject Headings
Aging; Animals; Anti-Mullerian Hormone; Base Sequence; DNA Probes; Female; Gene Expression; Gestational Age; *Glycoproteins; Growth Inhibitors; Male; Molecular Sequence Data; Mullerian Ducts; Oligonucleotide Probes; Poly A; Pregnancy; RNA, Messenger; Rats; Rats, Inbred Strains; Testicular Hormones; Testis; *Transcription, Genetic
Cell Biology | Developmental Biology | Endocrinology
Mullerian inhibiting substance (MIS) is a 140-kilodalton homodimeric glycoprotein that causes regression of the Mullerian ducts in male embryos, and may also have a role in both males and females in the regulation of germ cell maturation. We examined the ontogeny of MIS messenger RNA (mRNA) in rat testes from midgestation through adulthood and found two discrete MIS mRNA species that are developmentally regulated. The larger 2.0-kilobase species is abundant at embryonic day 14, then decreases in late gestation, and is barely detectable after birth. The smaller 1.8-kilobase species is first noted at embryonic day 18 and is the major species detected postnatally. Both species are abundant just prior to birth, at embryonic day 21, then decrease markedly after birth. This variation in MIS mRNA levels correlates with the developmental expression of MIS protein. A series of oligonucleotide-directed ribonuclease H mapping experiments determined that the two mRNA species differ at their 3' ends in the extent of polyadenylation. Thus, differential polyadenylation of MIS mRNA may be an additional mechanism for regulating MIS expression during fetal and postnatal development.
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Citation: Endocrinology. 1992 Feb;130(2):847-53. Link to article on publisher's site
Lee, Mary M.; Cate, Richard L.; Donahoe, Patricia K.; and Waneck, Gerald L., "Developmentally regulated polyadenylation of two discrete messenger ribonucleic acids for mullerian inhibiting substance" (1992). Lee Lab Publications. 28.