Abstract:
:Activity of acetyl-CoA carboxylase (ACC)-alpha is rate limiting for de novo synthesis of fatty acids. The encoding gene is expressed by three different promoters. We characterized promoter III (PIII) from cow, previously only known from sheep. Quantitation of transcripts by RNAse protection assays and real time PCR revealed that PIII is primarily expressed and strongly induced ( approximately 28-fold) in the lactating mammary gland. PIII transcripts are expressed in mammary epithelial cells (MEC) as shown by in situ hybridization. A 2999 bp segment of the PIII promoter conferred prolactin and dexamethasone inducibility to a luciferase reporter gene in stably transfected mouse MEC cells. Lactogenic induction was abolished if a unique signal transducer and activator of transcription (STAT)-binding site at position -797 was inactivated by two point mutations. An oligonucleotide probe harboring this STAT-site specifically bound nuclear proteins from the lactating mammary gland. Binding was abolished by those two point mutations and super-shift analyses showed that STAT5A factors are present in this complex. Hence, prolactin, acting through STAT5, contributes to the activation of ACC expression in the milk producing cells of the lactating mammary gland. We discuss that STAT5 might be important in determining the milk composition by coordinating fatty acid and protein synthesis during lactation.
journal_name
J Mol Endocrinoljournal_title
Journal of molecular endocrinologyauthors
Mao J,Molenaar AJ,Wheeler TT,Seyfert HMdoi
10.1677/jme.0.0290073subject
Has Abstractpub_date
2002-08-01 00:00:00pages
73-88issue
1eissn
0952-5041issn
1479-6813pii
JME01113journal_volume
29pub_type
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