首页> 外文期刊>Plant, Cell & Environment >An inhibitory effect of the sequence-conserved upstream open-reading frame on the translation of the main open-reading frame of HsfB1 transcripts in Arabidopsis. (Virtual special issue on whole-plant water transport.)
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An inhibitory effect of the sequence-conserved upstream open-reading frame on the translation of the main open-reading frame of HsfB1 transcripts in Arabidopsis. (Virtual special issue on whole-plant water transport.)

机译:序列保守的上游开放阅读框对拟南芥中HsfB1转录本主要开放阅读框翻译的抑制作用。 (有关全厂水运输的虚拟特刊。)

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摘要

Plants have as many as 20 heat shock factors (Hsfs) grouped into three classes, A, B and C, based on sequence similarity and modular structures. Through screening for cell death-inducing factor(s) in Nicotiana benthamiana, we identified Arabidopsis HsfB2b and thus subjected all other members of Arabidopsis Hsf class B (HsfB1, HsfB2a, HsfB2b, HsfB3 and HsfB4) to the same cell death assay. When expressed in N. benthamiana leaves, only HsfB1 and HsfB2b elicited mild cell death. Simultaneously we found that HsfB1 has a post-transcriptional control mechanism, in which a sequence-conserved upstream open-reading frame (sc-uORF) is involved. The known repressor function of the respective HsfBs was confirmed and the difference in cell death-inducing activity of HsfBs was explained by the fact that HsfB1 and HsfB2b are transcriptional repressors but the others are not. Indeed, the cell death symptom by HsfB1 and HsfB2b required not only their repression activity but also their nuclear localization activity. HsfB1 expression was drastically and transiently induced by heat shock (HS) and the intactness of sc-uORF was required for its HS response. Based on the results, the physiological significance of cell death-inducing activity of HsfB1 and HsfB2b and the sc-uORF in the HsfB1 transcript during HS response is discussed.
机译:根据序列相似性和模块化结构,植物可将多达20种热冲击因子(Hsfs)分为A,B和C三类。通过筛选本生烟草中的细胞死亡诱导因子,我们鉴定了拟南芥HsfB2b,从而使拟南芥Hsf B类的所有其他成员(HsfB1,HsfB2a,HsfB2b,HsfB3和HsfB4)进行相同的细胞死亡测定。当在本氏烟草叶中表达时,只有HsfB1和HsfB2b引起轻度细胞死亡。同时,我们发现HsfB1具有转录后控制机制,其中涉及序列保守的上游开放阅读框(sc-uORF)。证实了各个HsfB的已知阻遏物功能,并且HsfB1和HsfB2b是转录阻遏物,而其他HsfB1b却不是转录阻遏物,从而解释了HsfBs在细胞死亡诱导活性上的差异。实际上,HsfB1和HsfB2b引起的细胞死亡症状不仅需要其抑制活性,还需要其核定位活性。 HsfB1表达被热休克(HS)彻底和短暂地诱导,sc-uORF的完整需要HS响应。根据这些结果,探讨了HS应答中HsfB1和HsfB2b以及sc-uORF中HsfB1和HsfB2b的细胞死亡诱导活性的生理意义。

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