CLE肽通过受体样激酶CRINKLY 4作用于Physcomitrium patens配子体的发育。

Plant signaling & behavior Pub Date : 2024-12-31 Epub Date: 2024-07-31 DOI:10.1080/15592324.2024.2386502
Alain Shumbusho, C Jill Harrison, Viktor Demko
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引用次数: 0

摘要

CLAVATA 通路在有花植物多细胞芽和根分生组织的调控中起着关键作用。在拟南芥中,CLAVATA 3 样信号肽(CLEs)通过受体样激酶 CLAVATA 1 和 CRINKLY 4(CR4)发挥作用。以前曾对青苔 Physcomitrium patens 中的 PpCLAVATA 和 PpCR4 进行过独立研究,结果表明它们在细胞增殖和分化调控中发挥着一致的作用。植物钙蛋白酶 DEFECTIVE KERNEL 1(DEK1)已被确定为维管束植物和裸子植物中细胞分裂和细胞命运的另一个关键调控因子。CLAVATA、CR4 和 DEK1 之间的功能性相互作用仍然未知。在这里,我们发现 P. patens crinkly4 和 dek1 突变体对 CLE 肽处理的反应不同,这表明它们在 CLAVATA 通路中发挥着不同的作用。在 Δcr4 突变体中,CLAVATA 介导的叶芽生长抑制作用降低,这表明 PpCR4 参与了 CLV3p 的感知,很可能是作为受体。CLV3p 强烈抑制了 Δcr4 突变体中的叶脉发育,这表明其他受体也参与了这些过程,并表明 PpCR4 在器官对 CLE 的敏感性中的潜在作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
CLE peptides act via the receptor-like kinase CRINKLY 4 in Physcomitrium patens gametophore development.

The CLAVATA pathway plays a key role in the regulation of multicellular shoot and root meristems in flowering plants. In Arabidopsis, CLAVATA 3-like signaling peptides (CLEs) act via receptor-like kinases CLAVATA 1 and CRINKLY 4 (CR4). In the moss Physcomitrium patens, PpCLAVATA and PpCR4 were previously studied independently and shown to play conserved roles in the regulation of cell proliferation and differentiation. The plant calpain DEFECTIVE KERNEL 1 (DEK1) has been identified as another key regulator of cell division and cell fate in vascular plants and bryophytes. The functional interaction between CLAVATA, CR4, and DEK1 remains unknown. Here, we show that P. patens crinkly4 and dek1 mutants respond differently to CLE peptide treatments suggesting their distinct roles in the CLAVATA pathway. Reduced CLAVATA-mediated suppression of leafy shoot growth in Δcr4 mutants indicates that PpCR4 is involved in CLV3p perception, most likely as a receptor. The CLV3p strongly suppressed leaf vein development in Δcr4 mutants, suggesting that other receptors are involved in these processes and indicating a potential role of PpCR4 in organ sensitization to CLEs.

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