Mozgová Iva, Muñoz-Viana Rafael, Hennig Lars
Department of Plant Biology, Uppsala BioCenter, Swedish University of Agricultural Sciences and Linnean Center for Plant Biology, Uppsala, Sweden.
Institute of Microbiology, Centre Algatech, Opatovický mlýn, Třeboň, Czech Republic.
PLoS Genet. 2017 Jan 17;13(1):e1006562. doi: 10.1371/journal.pgen.1006562. eCollection 2017 Jan.
Many plant cells can be reprogrammed into a pluripotent state that allows ectopic organ development. Inducing totipotent states to stimulate somatic embryo (SE) development is, however, challenging due to insufficient understanding of molecular barriers that prevent somatic cell dedifferentiation. Here we show that Polycomb repressive complex 2 (PRC2)-activity imposes a barrier to hormone-mediated transcriptional reprogramming towards somatic embryogenesis in vegetative tissue of Arabidopsis thaliana. We identify factors that enable SE development in PRC2-depleted shoot and root tissue and demonstrate that the establishment of embryogenic potential is marked by ectopic co-activation of crucial developmental regulators that specify shoot, root and embryo identity. Using inducible activation of PRC2 in PRC2-depleted cells, we demonstrate that transient reduction of PRC2 activity is sufficient for SE formation. We suggest that modulation of PRC2 activity in plant vegetative tissue combined with targeted activation of developmental pathways will open possibilities for novel approaches to cell reprogramming.
许多植物细胞可以被重编程为多能状态，从而实现异位器官发育。然而，由于对阻止体细胞去分化的分子障碍了解不足，诱导全能状态以刺激体细胞胚胎（SE）发育具有挑战性。在这里，我们表明，多梳抑制复合体2（PRC2）的活性对拟南芥营养组织中激素介导的向体细胞胚胎发生的转录重编程形成了障碍。我们鉴定了在PRC2缺失的茎和根组织中促成SE发育的因子，并证明胚胎发生潜能的建立以指定茎、根和胚胎身份的关键发育调节因子的异位共激活为特征。通过在PRC2缺失的细胞中诱导激活PRC2，我们证明PRC2活性的短暂降低足以形成SE。我们认为，调节植物营养组织中PRC2的活性并结合发育途径的靶向激活，将为细胞重编程的新方法开辟可能性。
