愈伤组织诱导是植物体细胞再生的关键。近期研究表明，生长素诱导的愈伤组织起源于中柱鞘细胞或类中柱鞘细胞,经过类似于根发育的程序获得干细胞特性及再生能力。然而，控制中柱鞘细胞愈伤组织形成分生能力的分子机制仍不清楚。通过特异筛选根部成熟区连贯性形成愈伤组织的突变体，我们发现编码WD40类蛋白的ECF1（Enhanced Callus Formation 1）突变导致整个根部中柱鞘细胞愈伤组织形成分生能力增强。本项目拟通过ECF1时空表达模式及根各层细胞命运分析，明确ECF1控制中柱鞘细胞愈伤组织形成分生能力的细胞学基础。进而分析愈伤组织诱导早期ECF1对中柱鞘细胞生长素及细胞分裂素响应、干细胞及细胞分生能力关键调控因子PLTs、ALF4等表达的影响，结合ECF1互作蛋白及其靶基因在调控中柱鞘愈伤组织形成分生能力方面功能鉴定，解析ECF1信号通路控制中柱鞘细胞愈伤组织形成分生能力的分子机制。

Callus induction is initial for plant somatic cell regeneration. Recent studies showed that auxin-induced callus formation originates from the pericycle or pericycle-like cells via a root developmental pathway to acquire stem cell characteristics and regeneration capacity. However, the underlying mechanisms governing pericycle cell competence for callus formation remain elusive. By specific screening of the mutants which form continuous layer of callus in root mature zone, we found that mutation of ECF1 (Enhanced Callus Formation 1), encoding the WD40-class protein, enhanced the pericycle cell competence for callus formation in the entire root. In this study, the spatiotemporal expression of ECF1 and the fate of root cells will be analyzed, thus to clarify the cytological basis of ECF1 in confining pericycle cell competence for callus formation. Further studies will be focused on the effects of ECF1 on auxin and cytokinin responses, as well as expression of key regulators of stem cell and cell competence, such as PLTs, ALF4, in the pericycle cells at the initial stage of callus induction. In combination with the identification of ECF1-interacting proteins and their target genes in the regulation of pericycle cell competence for callus formation, the molecular mechanism of pericycle cell competence for callus formation controlled by ECF1 signaling pathway will be elucidated.