内鞘細胞アイデンティティー決定の分子機構

我一直在筛选决定周细胞特性的关键转录因子。我的筛选已经发现了两个碱性螺旋-环-螺旋(BHLH)家族转录因子，以17号(包括17号、17H号、17H2号和17H3号)和51号(包括51号、36号、14号、14L号等)为代表，它们在调控周细胞的识别方面发挥着关键作用。酵母双杂交筛选证实了这两个蛋白分支之间的相互作用。第51号蛋白在周细胞中特异表达。第51号过表达(第51号-OE)导致XPP标记GFP的异位表达。重要的是，51-OE引起了根细胞的异位分裂。外源生长素促进了51-OE根的异位细胞分裂，表明51号具有进行生长素诱导的细胞分裂的能力。17号OE的表型与51号相似，但程度较轻。17号在几种细胞类型中广泛表达，包括中柱细胞。51号调控17号S转录，但反之亦然。51路也是自动调节的。这样的反馈加强了他们自己的转录。51‘OE根的转录图谱表明，51’OE根上调了许多中柱细胞特异基因的表达，提示51‘S对中柱细胞的识别起正向调控作用。对获得的第51-OE/第51-SRDX根的转录图谱的详细分析将有助于鉴定bHLHTFS的下游效应子。

I have been screening for the key transcription factors that determine pericycle cell Identity. My screening has revealed two clades of basic Helix-Loop-Helix (bHLH) family transcription factors, represented by No.17 (including No.17, No.17H, No.17H2, and No.17H3) and No. 51 (including No.51, No. 36, No.14, No.14L etc.), that play key roles in regulation pericycle cell identity. A Yeast-Two-Hybrid screening confirmed the interaction between the two clades of proteins.No.51 is expressed specifically in pericycle cells. No.51 overexpression (No.51-OE) causes ectopic expression of XPP-marker GFP. Importantly, No.51-OE caused ectopic cell division in the root. Exogenous auxin increased the ectopic cell division in No.51-OE root, demonstrating that No.51 confers the competency to undergo auxin-induced cell division. No.17-OE caused similar but milder phenotype than that of No.51. No.17 is broadly expressed in several cell types including pericycle.No.51 regulate No.17's transcription, but not vice versa. No.51 is also auto-regulated. Such feedback reinforces their own transcription. No.51’s specific expression pattern confines this network in the pericycle, which constitutes a master regulation of pericycle cell’s identity.Transcriptional profiling of No.51-OE root shows that many pericycle-specific genes are up-regulated by No.51-OE, suggesting No.51’s role as a positive regulator of pericycle cell identity. Detailed analysis on the obtained transcriptional profile of No.51-OE/ No.51-SRDX roots will shed light on the identification of the bHLH TFs’ downstream effectors.