کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5906360 | 1159970 | 2013 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Poly(ADP-ribose) glycohydrolase and poly(ADP-ribose)-interacting protein Hrp38 regulate pattern formation during Drosophila eye development
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کلمات کلیدی
UASRetinitis pigmentosaGSCDE-cadherinPARP1ISESRD1PARG5′ Untranslated region - 5 'منطقه غیر ترجمه5′UTR - 5'UTRPoly(ADP-ribosyl)ation - Poly (ADP-ribosyl) ationPattern formation - تشکیل الگوExonic splicing enhancers - تقویت کننده های اسپلایسینگ اکسونEye development - توسعه چشمupstream activation sequence - دنباله فعال سازی بالادستHeterogeneous nuclear ribonucleoproteins - ریبونولوپروتئین های هسته ای ناهمگنGermline Stem Cell - سلول بنیادی گیاهیExonic splicing silencers - صدا خفه کن های اسپلیکسونDrosophila - مگس سرکهpADPr - پدریSR protein - پروتئین SRPoly(ADP-ribose) - پلی (ADP-ribose)Poly(ADP-ribose) polymerase 1 - پلی (ADP-ribose) پلیمراز 1Deficiency - کمبودESES - کهpoly(ADP-ribose) glycohydrolase - گلیکا هیدرولاز پلی (ADP-ribose)
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Drosophila Hrp38, a homolog of human hnRNP A1, has been shown to regulate splicing, but its function can be modified by poly(ADP-ribosyl)ation. Notwithstanding such findings, our understanding of the roles of poly(ADP-ribosyl)ated Hrp38 on development is limited. Here, we have demonstrated that Hrp38 is essential for fly eye development based on a rough-eye phenotype with disorganized ommatidia observed in adult escapers of the hrp38 mutant. We also observed that poly(ADP-ribose) glycohydrolase (Parg) loss-of-function, which caused increased Hrp38 poly(ADP-ribosyl)ation, also resulted in the rough-eye phenotype with disrupted ommatidial lattice and reduced number of photoreceptor cells. In addition, ectopic expression of DE-cadherin, which is required for retinal morphogenesis, fully rescued the rough-eye phenotype of the hrp38 mutant. Similarly, Parg mutant eye clones had decreased expression level of DE-cadherin with orientation defects, which is reminiscent of DE-cadherin mutant eye phenotype. Therefore, our results suggest that Hrp38 poly(ADP-ribosyl)ation controls eye pattern formation via regulation of DE-cadherin expression, a finding which has implications for understanding the pathogenic mechanisms of Hrp38-related Fragile X syndrome and PARP1-related retinal degeneration diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 526, Issue 2, 10 September 2013, Pages 187-194
Journal: Gene - Volume 526, Issue 2, 10 September 2013, Pages 187-194
نویسندگان
Yingbiao Ji, Michael Jarnik, Alexei V. Tulin,