Nguyen Nguyen Hoai, Sng Benny Jian Rong, Chin Hui Jun, Choi Ian Kin Yuen, Yeo Hock Chuan, Jang In-Cheol
Temasek Life Sciences Laboratory, National University of Singapore, 1 Research Link, Singapore, 117604, Singapore.
Department of Biological Sciences, National University of Singapore, Singapore, 117543, Singapore.
Plant J. 2023 Nov;116(3):804-822. doi: 10.1111/tpj.16410. Epub 2023 Jul 31.
Vegetative shade causes an array of morphological changes in plants called shade avoidance syndrome, which includes hypocotyl and petiole elongation, leaf hyponasty, reduced leaf growth, early flowering and rapid senescence. Here, we show that loss-of-function mutations in HISTONE DEACETYLASE 9 (HDA9) attenuated the shade-induced hypocotyl elongation in Arabidopsis. However, the hda9 cotyledons and petioles under shade were not significantly different from those in wild-type, suggesting a specific function of HDA9 in hypocotyl elongation in response to shade. HDA9 expression levels were stable under shade and its protein was ubiquitously detected in cotyledon, hypocotyl and root. Organ-specific transcriptome analysis unraveled that shade induced a set of auxin-responsive genes, such as SMALL AUXIN UPREGULATED RNAs (SAURs) and AUXIN/INDOLE-3-ACETIC ACIDs (AUX/IAAs) and their induction was impaired in hda9-1 hypocotyls. In addition, HDA9 binding to loci of SAUR15/65, IAA5/6/19 and ACS4 was increased under shade. The genetic and organ-specific gene expression analyses further revealed that HDA9 may cooperate with PHYTOCHROME-INTERACTING FACTOR 4/7 in the regulation of shade-induced hypocotyl elongation. Furthermore, HDA9 and PIF7 proteins were found to interact together and thus it is suggested that PIF7 may recruit HDA9 to regulate the shade/auxin responsive genes in response to shade. Overall, our study unravels that HDA9 can work as one component of a hypocotyl-specific transcriptional regulatory machinery that activates the auxin response at the hypocotyl leading to the elongation of this organ under shade.
营养遮荫会导致植物出现一系列形态变化，即所谓的避荫综合征，其中包括下胚轴和叶柄伸长、叶片下弯、叶片生长受抑制、早花和快速衰老。在此，我们表明组蛋白去乙酰化酶9（HDA9）的功能缺失突变减弱了拟南芥中遮荫诱导的下胚轴伸长。然而，遮荫条件下hda9的子叶和叶柄与野生型并无显著差异，这表明HDA9在响应遮荫时的下胚轴伸长中具有特定功能。HDA9的表达水平在遮荫条件下保持稳定，其蛋白在子叶、下胚轴和根中均能普遍检测到。器官特异性转录组分析表明，遮荫诱导了一组生长素响应基因，如小生长素上调RNA（SAURs）和生长素/吲哚-3-乙酸（AUX/IAAs），而hda9-1下胚轴中这些基因的诱导受到损害。此外，在遮荫条件下，HDA9与SAUR15/65、IAA5/6/19和ACS4基因座的结合增加。遗传和器官特异性基因表达分析进一步表明，HDA9可能与光敏色素相互作用因子4/7协同调节遮荫诱导的下胚轴伸长。此外，发现HDA9和PIF7蛋白相互作用，因此推测PIF7可能招募HDA9来调节响应遮荫的遮荫/生长素响应基因。总体而言，我们的研究表明，HDA9可作为下胚轴特异性转录调控机制的一个组成部分，该机制激活下胚轴的生长素反应，导致该器官在遮荫条件下伸长。
