Very-long-chain fatty acids restrict regeneration capacity by confining pericycle competence for callus formation in Arabidopsis
Very-long-chain fatty acids restrict regeneration capacity by confining pericycle competence for callus formation in Arabidopsis
复制标题
超长链脂肪酸通过限制拟南芥愈伤组织形成的中柱鞘能力来限制再生能力
DOI:
10.1073/pnas.1522466113
复制
发表时间:
2016-05-03
影响因子:
11.1
通讯作者:
Hu, Yuxin
中科院分区:
文献类型:
--
作者:
Shang, Baoshuan;Xu, Chongyi;Hu, Yuxin
Significance Callus induction is an initial step for typical plant in vitro regeneration, and recent studies show that auxin-induced callus formation in multiple organs occurs from the pericycle or pericycle-like cells via a root developmental pathway. We demonstrate here that very-long-chain fatty acids (VLCFAs) or their derivatives act as the critical signal in restricting the callus-forming capacity of the pericycle and thus the regeneration capability in Arabidopsis. Our work not only discloses an unidentified role of VLCFAs in defining the regeneration capacity, but also sheds light on the signals that govern the cell states in plant organs. Our findings also may have relevance for investigating the possible role of VLCFAs in the regulation of cell states in animals. 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.