AT-rich repetitive DNA sequences, transcription frequency and germ layer determination. (November 2015)

• Record Type: Journal Article
• Authors: Flickinger, Reed
• Is Part Of: Mechanisms of development. Volume 138 Part 3(2015)
• Page Start: 227
• Page End: 232
• Publication Date: 2015-11
• Subjects: Germ layer determination -- AT-rich DNA; Developmental biology -- Periodicals; Molecular biology -- Periodicals; Developmental Biology -- Periodicals; Molecular Biology -- Periodicals; Biologie du développement -- Périodiques; Biologie moléculaire -- Périodiques; Developmental biology; Molecular biology; Periodicals; Electronic journals; 571.8
• DOI: 10.1016/j.mod.2015.10.004
• Languages: English
• ISSNs: 0925-4773

Abstract

Abstract: Non-coding sequences of frog embryo endoderm poly (A +) nuclear RNA are AU-enriched, as compared to those of ectoderm and mesoderm. Endoderm blastomeres contain much less H1 histone than is present in ectoderm and mesoderm. H1 histone preferentially binds AT-rich DNA sequences to repress their transcription. The AT-enrichment of non-coding DNA sequences transcribed into poly (A +) nuclear RNA, as well as the low amount of H1 histone, may contribute to the higher transcription frequency of mRNA of endoderm, as compared to that of ectoderm and mesoderm. A greater accumulation of H1 histone in presumptive mesoderm and ectoderm may prevent transcription of endoderm specifying genes in mesoderm and ectoderm. Experimental upregulation of various transcription factors (TFs) can redirect germ layer fate. Most of these TFs bind AT-rich consensus sequences in DNA, suggesting that H1 histone and TFs active during germ layer determination are binding similar sequences. Highlights: Amphibian embryo endoderm transcribes more mRNA per cell than ectoderm and mesoderm. Low H1 histone allows greater transcription from endoderm blastomeres. More H1 histone in ectoderm and mesoderm prevents endoderm-specific gene expression. Regulatory proteins bind similar AT-rich repeats in germ layer determination. There is a restriction of transcription of AT-rich repeats during early development.