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The splicing factor prp31 is essential for photoreceptor development in Drosophila

Protein & Cell 2010年第3期1卷 267-274页

作者： Payal Ray Xiaoyan Luo Elizabeth J.Rao Amina Basha Elvin A.Woodruff III Jane Y.Wu Department of Neurology Northwestern University Feinberg Medical SchoolChicagoIL 60611USA Magnify Inc. 2316 Riverside DrNashvilleTN 37216USA Present address:Trumbull College Yale UniversityNew HavenCT 06511USA

Retinitis pigmentosa is a leading cause of blindness and a progressive retinal disorder,affecting millions of people *** disease is characterized by photoreceptor degeneration,eventually leading to complete *** dominant(adRP)has been associated with mutations in at least four ubiquitously expressed genes encoding pre-mRNA splicing factors—prp3,prp8,prp31 and *** function of adRPassociated splicing factor genes and molecular mechanisms by which mutations in these genes cause cell-type specific photoreceptor degeneration in humans remain to be *** investigate the in vivo function of these adRP-associated splicing factor genes,we examined Drosophila in which expression of fly prp31 homolog was *** analyses show that CG6876 is the likely candidate of Drosophila melanogaster prp31 homolog(Dmprp31).Predicted peptide sequence for CG6876 shows 57%similarity to the Homo sapiens prp31 protein(Hsprp31).Reduction of the endogenous prp31 by RNAi-mediated knockdown speci-fically in the eye leads to reduction of eye size or complete absence of eyes with remarkable features of photoreceptor degeneration and recapitulates the bimodal expressivity of human prp31 mutations in adRP *** transgenic Dmprp31RNAi flies provide a useful tool for identifying genetic modifiers or interacting genes for *** of the human prp31 in these animals leads to a partial rescue of the eye *** results indicate that the Drosophila CG6876 is the fly ortholog of mammalian prp31 gene.

关键词： Drosophila photoreceptor degeneration retinitis pigmentosa prp31

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The Splicing Factor prp31 Is Involved in Transcriptional Gene Silencing and Stress Response in Arabidopsis

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Molecular Plant 2015年第7期8卷 1053-1068页

作者： Jin-Lu Du Su-Wei Zhang Huan-Wei Huang Tao Cai Lin Li She Chen Xin-Jian He College of Life Sciences Beijing Normal University Beijing 100875 China National Institute of Biological Sciences Beijing 102206 China

Although DNA methylation is known to play an important role in the silencing of transposable elements （TEs） and introduced transgenes, the mechanisms that generate DNA methylation-independent transcrip- tional silencing are poorly understood. Previous studies suggest that RNA-directed DNA methylation （RdDM） is required for the silencing of the RD29A-LUC transgene in the Arabidopsis rosl mutant back- ground with defective DNA demethylase. Loss of function of ARGONAUTE 4 （AGO4） gene, which encodes a core RdDM component, partially released the silencing of RD29A-LUC in the rosl/ago4 double mutant plants. A forward genetic screen was performed to identify the mutants with elevated RD29A-LUC trans- gene expression in the rosl/ago4 mutant background. We identified a mutation in the homologous gene of prp31, which encodes a conserved pre-mRNA splicing factor that regulates the formation of the U4/ U6.U5 snRNP complex in fungi and animals. We previously demonstrated that the splicing factors ZOP1 and STA1 contribute to transcriptional gene silencing. Here, we reveal that Arabidopsis prp31 associates with ZOP1, STA1, and several other splicing-related proteins, suggesting that these splicing factors are both physically and functionally connected. We show that Arabidopsis prp31 participates in transcrip- tional gene silencing. Moreover, we report that prp31, STA1, and ZOP1 are required for development and stress response. Under cold stress, prp31 is not only necessary for pre-mRNA splicing but also for regulation of cold-responsive gene expression. Our results suggest that the splicing machinery has multiple functions including pre-mRNA splicing, gene regulation, transcriptional gene silencing, and stress response.

关键词： prp31 splicing factor DNA methylation transcriptional gene silencing stress response

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