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植物损伤激活 Ca 依赖性效应蛋白酶以释放免疫调节肽。

Damage on plants activates Ca-dependent metacaspases for release of immunomodulatory peptides.

机构信息

Zürich-Basel Plant Science Center, Department of Environmental Sciences, Botany, University of Basel, 4056 Basel, Switzerland.

Department of Plant Biotechnology and Bioinformatics, Ghent University, 9052 Ghent, Belgium.

出版信息

Science. 2019 Mar 22;363(6433). doi: 10.1126/science.aar7486.

Abstract

Physical damage to cells leads to the release of immunomodulatory peptides to elicit a wound defense response in the surrounding tissue. In , the plant elicitor peptide 1 (Pep1) is processed from its protein precursor, PRECURSOR OF PEP1 (PROPEP1). We demonstrate that upon damage, both at the tissue and single-cell levels, the cysteine protease METACASPASE4 (MC4) is instantly and spatiotemporally activated by binding high levels of Ca and is necessary and sufficient for Pep1 maturation. Cytosol-localized PROPEP1 and MC4 react only after loss of plasma membrane integrity and prolonged extracellular Ca entry. Our results reveal that a robust mechanism consisting of conserved molecular components links the intracellular and Ca-dependent activation of a specific cysteine protease with the maturation of damage-induced wound defense signals.

摘要

细胞的物理损伤会导致免疫调节肽的释放,从而在周围组织中引发伤口防御反应。在植物中,植物激发肽 1(Pep1)是从其蛋白质前体 PRECURSOR OF PEP1(PROPEP1)中加工而来的。我们证明,在组织和单细胞水平上受到损伤时,半胱氨酸蛋白酶 METACASPASE4(MC4)通过结合高水平的 Ca 立即被瞬时且时空激活,并且对于 Pep1 的成熟是必需且充分的。细胞质定位的 PROPEP1 和 MC4 仅在质膜完整性丧失和细胞外 Ca 进入延长后才反应。我们的结果表明,一种由保守的分子成分组成的强大机制将特定半胱氨酸蛋白酶的细胞内和 Ca 依赖性激活与损伤诱导的伤口防御信号的成熟联系起来。

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