Shang Baoshuan, Xu Chongyi, Zhang Xixi, Cao Huifen, Xin Wei, Hu Yuxin
Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China; University of the Chinese Academy of Sciences, Beijing 100049, China;
Key Laboratory of Plant Molecular Physiology, CAS Center for Excellence in Molecular Plant Sciences, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China;
Proc Natl Acad Sci U S A. 2016 May 3;113(18):5101-6. doi: 10.1073/pnas.1522466113. Epub 2016 Apr 18.
The already differentiated organs in plants have a remarkable capacity to regenerate new individuals under culture conditions. Plant in vitro regeneration practically starts with the induction of a pluripotent cell mass, the callus, from detached organs on auxin-rich callus-inducing medium (CIM), which is generally required for subsequent regeneration of new bodies. Recent studies show that CIM-induced callus formation occurs from the pericycle or pericycle-like cells through a root developmental pathway, whereas the signals involved in governing callus-forming capacity of pericycle cells remain unknown. Here we report that very-long-chain fatty acids (VLCFAs) play a critical role in confining the pericycle competence for callus formation and thus the regeneration capacity of Arabidopsis By genetic screening, we identified the callus formation-related 1 (cfr1) mutant, which bypasses the inhibition of callus-forming capacity in roots by solitary-root (slr/iaa14). We show that CFR1 encodes 3-ketoacyl-CoA synthase 1 (KCS1), which catalyzes a rate-limiting step of VLCFA biosynthesis. Our biochemical and genetic analyses demonstrate that VLCFAs restrict the pericycle competence for callus formation, at least in part, by regulating the transcription of Aberrant Lateral Root Formation 4 (ALF4). Moreover, we provide evidence that VLCFAs act as cell layer signals to mediate the pericycle competence for callus formation. Taken together, our results identify VLCFAs or their derivatives as the confining signals for mediating the pericycle competence for callus formation and thus the regeneration capacity of plant organs.
植物中已经分化的器官在培养条件下具有再生新个体的显著能力。植物离体再生实际上始于在富含生长素的愈伤组织诱导培养基（CIM）上从离体器官诱导出多能细胞团，即愈伤组织，这是后续新个体再生通常所需的。最近的研究表明，CIM诱导的愈伤组织形成是通过根发育途径从周皮或类周皮细胞发生的，而调控周皮细胞愈伤组织形成能力的信号仍然未知。在此，我们报道极长链脂肪酸（VLCFA）在限制周皮形成愈伤组织的能力从而限制拟南芥的再生能力方面起关键作用。通过遗传筛选，我们鉴定出愈伤组织形成相关1（cfr1）突变体，它绕过了单根（slr/iaa14）对根愈伤组织形成能力的抑制。我们表明CFR1编码3-酮脂酰-CoA合酶1（KCS1），其催化VLCFA生物合成的限速步骤。我们的生化和遗传分析表明，VLCFA至少部分地通过调节异常侧根形成4（ALF4）的转录来限制周皮形成愈伤组织的能力。此外，我们提供证据表明VLCFA作为细胞层信号来介导周皮形成愈伤组织的能力。综上所述，我们的结果确定VLCFA或其衍生物是介导周皮形成愈伤组织能力从而介导植物器官再生能力的限制信号。
