Kleine Tatjana, Kindgren Peter, Benedict Catherine, Hendrickson Luke, Strand Asa
Umeå Plant Science Centre, Department of Plant Physiology, Umeå University, Umeå, Sweden.
Plant Physiol. 2007 Jul;144(3):1391-406. doi: 10.1104/pp.107.098293. Epub 2007 May 3.
Exposure to high irradiance results in dramatic changes in nuclear gene expression in plants. However, little is known about the mechanisms by which changes in irradiance are sensed and how the information is transduced to the nucleus to initiate the genetic response. To investigate whether the photoreceptors are involved in the response to high irradiance, we analyzed expression of EARLY LIGHT-INDUCIBLE PROTEIN1 (ELIP1), ELIP2, ASCORBATE PEROXIDASE2 (APX2), and LIGHT-HARVESTING CHLOROPHYLL A/B-BINDING PROTEIN2.4 (LHCB2.4) in the phytochrome A (phyA), phyB, cryptochrome1 (cry1), and cry2 photoreceptor mutants and long hypocotyl5 (hy5) and HY5 homolog (hyh) transcription factor mutants. Following exposure to high intensity white light for 3 h (1,000 mumol quanta m(-2) s(-1)) expression of ELIP1/2 and APX2 was strongly induced and LHCB2.4 expression repressed in wild type. The cry1 and hy5 mutants showed specific misregulation of ELIP1/2, and we show that the induction of ELIP1/2 expression is mediated via CRY1 in a blue light intensity-dependent manner. Furthermore, using the Affymetrix Arabidopsis (Arabidopsis thaliana) 24 K Gene-Chip, we showed that 77 of the high light-responsive genes are regulated via CRY1, and 26 of those genes were also HY5 dependent. As a consequence of the misregulation of these genes, the cry1 mutant displayed a high irradiance-sensitive phenotype with significant photoinactivation of photosystem II, indicated by reduced maximal fluorescence ratio. Thus, we describe a novel function of CRY1 in mediating plant responses to high irradiances that is essential to the induction of photoprotective mechanisms. This indicates that high irradiance can be sensed in a chloroplast-independent manner by a cytosolic/nucleic component.
暴露于高辐照度会导致植物核基因表达发生显著变化。然而,关于辐照度变化是如何被感知以及信息如何传递到细胞核以启动基因响应的机制,我们所知甚少。为了研究光感受器是否参与对高辐照度的响应,我们分析了早期光诱导蛋白1(ELIP1)、ELIP2、抗坏血酸过氧化物酶2(APX2)和光捕获叶绿素a/b结合蛋白2.4(LHCB2.4)在光敏色素A(phyA)、phyB、隐花色素1(cry1)和cry2光感受器突变体以及长下胚轴5(hy5)和HY5同源物(hyh)转录因子突变体中的表达情况。在暴露于高强度白光3小时(1000 μmol光子·m⁻²·s⁻¹)后,野生型中ELIP1/2和APX2的表达被强烈诱导,而LHCB2.4的表达受到抑制。cry1和hy5突变体显示出ELIP1/2的特异性调控异常,并且我们表明ELIP1/2表达的诱导是以蓝光强度依赖的方式通过CRY1介导的。此外,使用Affymetrix拟南芥24K基因芯片我们发现,77个高光响应基因是通过CRY1调控的,其中26个基因也依赖于HY5。由于这些基因的调控异常,cry1突变体表现出高辐照度敏感表型,光系统II发生显著的光失活,这通过最大荧光比值降低得以表明。因此,我们描述了CRY1在介导植物对高辐照度响应中的一种新功能,这对于光保护机制的诱导至关重要。这表明高辐照度可以通过胞质/核成分以不依赖叶绿体的方式被感知。