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首页> 外文期刊>Biochemistry >Signaling Mechanisms Regulating Diverse Plant Cell Responses to UVB Radiation
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Signaling Mechanisms Regulating Diverse Plant Cell Responses to UVB Radiation

机译:调节不同植物细胞对UVB辐射的传导机制

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UVB radiation (290-320 nm) causes diverse effects in plant cells that vary with the fluence rate of exposure. High fluence rates of UVB radiation cause damage to DNA and formation of reactive oxygen species in mitochondria and chloroplasts, which lead to oxidation of membrane proteins and lipids and inhibition of cellular functions. In response to oxidative stress, mitochondrial transmembrane potential dissipates, resulting in cytochrome c release and activation of metacaspases. This leads to the apoptosis-like cell death. The signaling mechanism based on UVB DNA damage includes check-point activation, cell-cycle arrest, and finally programmed cell death with characteristic DNA fragmentation and morphological hallmarks typical of apoptotic cells. Recently, it was shown that among the components of this signaling mechanism the transcriptional factor SOG1 (suppressor of gamma response 1) plays a key role in regulation of programmed cell death in plants. In contrast to its damaging effects, UVB radiation at low fluence rates can act as a regulatory signal that is specifically perceived by plants to promote acclimation and survival in sunlight. The protective action of UVB is based on expression of various genes, including those encoding flavonoid synthesis enzymes that provide a UVB-absorbing sunscreen in epidermal tissues and DNA photorepair enzymes. These processes are mediated by the UVB photoreceptor UVR8, which has been recently characterized at the molecular level. Now progress is made in uncovering the UVR8-mediated signaling path-way mechanism in the context of UVB photon perception and revealing the biochemical components of the early stages of light signal transduction. In this review, attention is focused on the achievements in studying these UVB-induced signaling processes.
机译:UVB辐射(290-320nm)在植物细胞中导致不同的植物细胞效果,这些植物细胞随着曝光率的流量而变化。高流量的UVB辐射率导致DNA损伤和线粒体和叶绿体中的反应性氧物种的形成,这导致膜蛋白和脂质的氧化和细胞功能的抑制。响应于氧化应激,线粒体跨膜电位耗散,导致细胞色素C释放和选叠酶活化。这导致细胞凋亡样细胞死亡。基于UVB DNA损伤的信号机制包括检查点激活,细胞周期停滞,并且最后编程细胞死亡,具有典型的凋亡细胞的特征DNA碎片和形态标志。最近,表明该信号调查的组分中的转录因子Sog1(γ响应1的抑制剂1)在植物中编程细胞死亡的调节中起着关键作用。与其损坏的效果相比,低流量率的UVB辐射可以作为植物特别感知的调节信号,以促进阳光下的适应和生存。 UVB的保护作用是基于各种基因的表达,包括编码类黄酮合成酶的那些,该酶在表皮组织和DNA光磷脂酶中提供UVB吸收的防晒剂。这些过程由UVB光感受器UVR8介导,该UVR8最近已经表征在分子水平。现在在UVB光子感知的背景下揭示UVR8介导的信号路径机制并揭示光信号转导早期阶段的生物化学成分的研究进展。在本次审查中,关注研究这些UVB诱导的信令过程的成就。

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