Chlorophyll Metabolism and Its Role in Responses and Adaptations to Stress

生物 程序性细胞死亡 叶绿体 质体 活性氧 非生物成分 分解代谢 叶绿素 细胞生物学 生物化学 光防护 黄化 衰老 新陈代谢 光合作用 植物 细胞凋亡 基因 古生物学
作者
Luis A. J. Mur,Helen Ougham,Howard Thomas
标识
DOI:10.1002/9781119312994.apr0785
摘要

Abstract This article discusses the role of chlorophyll metabolism in plant responses and adaptations to biotic and abiotic stresses. The metabolic pathways of chlorophyll (Chl) biosynthesis and catabolism are summarised. The precursor of tetrapyrrole synthesis is δ‐aminolaevulinic acid. Protoporphyrin IX is the branchpoint intermediate between the haem/bilin route and the direction leading to Chl. Disrupting individual steps in the biosynthetic pathway generally results in accumulation of phototoxic intermediates, damage by reactive oxygen species (ROS), light‐dependent cell death and tissue lesions. Mutations in the haem branch do not usually lead to lesion formation but can have a regulatory influence on Chl metabolism. The Chl a/b cycle links pigment synthesis and catabolism. The initial steps of Chl breakdown during senescence occur in the plastid and result in export of phyllobilins to the cytosol and vacuole. Disabling steps in the plastid pathway results in photosensitivity and runaway cell damage and death. Common plant responses to environmental stresses include chlorosis, cell death and premature senescence, and biotic and abiotic challenges frequently share aspects of underlying signal‐response networks. Resurrection plants and overwintering evergreens are discussed as case studies of the sensitivity of Chl metabolism to abiotic stresses. Responses to high light and temperature involve Chl catabolism, ROS, and pathways of chloroplast breakdown, including autophagy and vesiculation. In many instances, single‐gene and quantitative resistance to pathogens elicit a hypersensitive response (HR), involving a burst of ROS and localised cell death. Accumulated photodynamic intermediates of Chl metabolism are important sources of ROS in these contexts. Lines in which genes for Chl catabolism are overexpressed or disabled display enhanced or suppressed HR‐like symptoms respectively, and correspondingly resistant or susceptible reactions to biotic, and in some cases abiotic, challenges.
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