PHB3 regulates lateral root primordia formation via NO-mediated degradation of AUXIN/INDOLE-3-ACETIC ACID proteins
PHB3 regulates lateral root primordia formation via NO-mediated degradation of AUXIN/INDOLE-3-ACETIC ACID proteins
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DOI：
10.1093/jxb/erac115
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发表时间：
2022-04-30
影响因子：
6.9
通讯作者：
Wang, Yong
中科院分区：
文献类型：
--
作者：
Li, Shuna;Li, Qingqing;Wang, Yong
PHB3通过控制一氧化氮的积累来调控IAA28和IAA14的降解，从而调节侧根创始细胞的鉴定和不对称分裂。我们先前已经证明，拟南芥Prohibitin 3(PHB3)控制生长素刺激的侧根(LR)的形成；然而，其潜在的分子机制尚不清楚。在这里，我们证明了PHB3主要通过影响侧根原基(LRP)的启动，通过影响一氧化氮(NO)的积累来调节侧根(LR)的发育。用NO供体处理后，phb3突变体中减少的LRP在很大程度上被挽救。通过抑制吲哚-3-醋酸诱导的14/28(IAA14/28)的降解，phb3中NO的积累减少导致GATA转录因子23(GATA23)和侧器官边界结构域16(LBD16)的表达降低。在phb3突变背景中过表达GATA23或LBD16可以恢复LRP密度的降低。这些结果表明，PHB3通过NO介导的生长素信号通路，通过调节IAA14/28的降解来调节LRP的启动。
PHB3 regulates degradation of IAA28 and IAA14 by controlling nitric oxide accumulation, thereby regulating lateral root founder cell identification and asymmetric division.We have previously shown that Arabidopsis thaliana Prohibitin 3 (PHB3) controls auxin-stimulated lateral root (LR) formation; however, the underlying molecular mechanism is unknown. Here, we demonstrate that PHB3 regulates lateral root (LR) development mainly through influencing lateral root primordia (LRP) initiation, via affecting nitric oxide (NO) accumulation. The reduced LRP in phb3 mutant was largely rescued by treatment with a NO donor. The decreased NO accumulation in phb3 caused a lower expression of GATA TRANSCRIPTION FACTOR 23 (GATA23) and LATERAL ORGAN BOUNDARIES DOMAIN 16 (LBD16) through inhibiting the degradation of INDOLE-3-ACETIC ACID INDUCIBLE 14/28 (IAA14/28). Overexpression of either GATA23 or LBD16 in phb3 mutant background recovered the reduced density of LRP. These results indicate that PHB3 regulates LRP initiation via NO-mediated auxin signalling, by modulating the degradation of IAA14/28.