Fraikin G Ya
Lomonosov Moscow State University, Moscow, 119991, Russia.
Biochemistry (Mosc). 2018 Jul;83(7):787-794. doi: 10.1134/S0006297918070027.
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 checkpoint 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 pathway 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.
紫外线B辐射(290 - 320纳米)在植物细胞中会产生多种效应,这些效应会随着照射通量率的变化而不同。高通量率的紫外线B辐射会对DNA造成损伤,并在线粒体和叶绿体中形成活性氧,这会导致膜蛋白和脂质的氧化以及细胞功能的抑制。作为对氧化应激的响应,线粒体跨膜电位消散,导致细胞色素c释放和metacaspases的激活。这会导致类似凋亡的细胞死亡。基于紫外线B对DNA损伤的信号传导机制包括检查点激活、细胞周期停滞,最终导致程序性细胞死亡,并伴有典型的DNA片段化和凋亡细胞特有的形态学特征。最近的研究表明,在这一信号传导机制的组成部分中,转录因子SOG1(γ反应抑制因子1)在植物程序性细胞死亡的调控中起关键作用。与其破坏作用相反,低通量率的紫外线B辐射可以作为一种调控信号,被植物特异性地感知,以促进其在阳光下的适应和存活。紫外线B的保护作用基于各种基因的表达,包括那些编码黄酮类合成酶的基因,这些酶在表皮组织中提供吸收紫外线B的防晒剂以及DNA光修复酶。这些过程由紫外线B光受体UVR8介导,最近已在分子水平上对其进行了表征。目前,在揭示UVR8介导的信号通路机制(在紫外线B光子感知的背景下)以及揭示光信号转导早期阶段的生化组成部分方面取得了进展。在这篇综述中,重点关注了在研究这些紫外线B诱导的信号传导过程方面所取得的成果。