کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9913649 | 1550642 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nanos downregulates transcription and modulates CTD phosphorylation in the soma of early Drosophila embryos
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Nanos downregulates transcription and modulates CTD phosphorylation in the soma of early Drosophila embryos Nanos downregulates transcription and modulates CTD phosphorylation in the soma of early Drosophila embryos](/preview/png/9913649.png)
چکیده انگلیسی
nanos (nos) specifies posterior development in the Drosophila embryo by repressing the translation of maternal hb mRNA. In addition to this somatic function, nos is required in the germline progenitors, the pole cells, to establish transcriptional quiescence. We have previously reported that nos is required to keep the Sex-lethal establishment promoter, Sxl-Pe, off in the germline of both sexes. We show here that nos also functions to repress Sxl-Pe activity in the surrounding soma. Sxl-Pe is inappropriately activated in the soma of male embryos from nos mothers, while Sxl-Pe can be repressed in female embryos by ectopic Nos protein. nos appears to play a global role in repressing transcription in the soma as the effects of nos on promoter activity are correlated with changes in the phosphorylation status of the carboxy terminal domain (CTD) repeats of the large RNA polymerase II subunit. Finally, we present evidence indicating that the suppression of transcription in the soma by Nos protein is important for normal embryonic development.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mechanisms of Development - Volume 122, Issue 5, May 2005, Pages 645-657
Journal: Mechanisms of Development - Volume 122, Issue 5, May 2005, Pages 645-657
نویسندگان
Girish Deshpande, Gretchen Calhoun, Timothy M. Jinks, Alexandros D. Polydorides, Paul Schedl,