Dynamic evolution of small signalling peptide compensation in plant stem cell control
Dynamic evolution of small signalling peptide compensation in plant stem cell control
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DOI：
10.1038/s41477-022-01118-w
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发表时间：
2022-03-28
期刊：
影响因子：
18
通讯作者：
Lippman, Zachary B.
中科院分区：
文献类型：
--
作者：
Kwon, Choon-Tak;Tang, Lingli;Lippman, Zachary B.
基因复制是植物基因组进化的标志，也是形成表型多样性的遗传相互作用的基础（1-5）。补偿是等位基因相互作用的一种主要形式（6-8），但补偿关系如何随着等位基因变异的积累而变化尚不清楚。在这里，我们利用整个茄科家族的基因组学和基因组编辑来捕获补偿旁系同源物的进化。干细胞调节剂CLV 3的突变导致许多植物的花器官过度增殖（9-11）。在番茄中，这种表型被密切相关的paraenoprotein的转录上调部分抑制（12）。烟草失去了这一优势，导致没有补偿和极端clv 3表型。引人注目的是，矮牵牛和地樱桃的旁系同源物几乎完全抑制了clv 3，表明了一种强有力的祖先补偿状态。跨物种的转基因互补分析表明，这种有效的补偿部分退化番茄由于一个单一的氨基酸的变化，顺式调节的变异，限制其转录上调。我们的研究结果显示了遗传相互作用是如何在复制后重塑的，并表明动态paradigm进化在短时间尺度上广泛存在，并影响来自自然和工程突变的表型变异。
Gene duplications are a hallmark of plant genome evolution and a foundation for genetic interactions that shape phenotypic diversity(1-5). Compensation is a major form of paralogue interactions(6-8) but how compensation relationships change as allelic variation accumulates is unknown. Here we leveraged genomics and genome editing across the Solanaceae family to capture the evolution of compensating paralogues. Mutations in the stem cell regulator CLV3 cause floral organs to overproliferate in many plants(9-11). In tomato, this phenotype is partially suppressed by transcriptional upregulation of a closely related paralogue(12). Tobacco lost this paralogue, resulting in no compensation and extreme clv3 phenotypes. Strikingly, the paralogues of petunia and groundcherry nearly completely suppress clv3, indicating a potent ancestral state of compensation. Cross-species transgenic complementation analyses show that this potent compensation partially degenerated in tomato due to a single amino acid change in the paralogue and cis-regulatory variation that limits its transcriptional upregulation. Our findings show how genetic interactions are remodelled following duplications and suggest that dynamic paralogue evolution is widespread over short time scales and impacts phenotypic variation from natural and engineered mutations.