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Reactive Oxygen Species Scavenging Enzymes and Down‐Adjustment of Metabolism Level in Mitochondria Associated with Desiccation‐Tolerance Acquisition of Maize Embryo
Author(s) -
Wu JingHua,
Wang WeiQing,
Song SongQuan,
Cheng HongYan
Publication year - 2009
Publication title -
journal of integrative plant biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.734
H-Index - 83
eISSN - 1744-7909
pISSN - 1672-9072
DOI - 10.1111/j.1744-7909.2009.00841.x
Subject(s) - reactive oxygen species , desiccation , desiccation tolerance , embryo , biology , mitochondrion , metabolism , enzyme , germination , botany , microbiology and biotechnology , biochemistry
It is a well‐known fact that a mature seed can survive losing most of its water, yet how seeds acquire desiccation‐tolerance is not well understood. Through sampling maize embryos of different developmental stages and comparatively studying the integrity, oxygen consumption rate and activities of antioxidant enzymes in the mitochondria, the main origin site of reactive oxygen species (ROS) production in seed cells, we found that before an embryo achieves desiccation‐tolerance, its mitochondria shows a more active metabolism, and might produce more ROS and therefore need a more effective ROS scavenging system. However, embryo dehydration in this developmental stage declined the activities of most main antioxidant enzymes and accumulated thiobarbituric acid‐reactive products in mitochondria, and then destroyed the structure and functional integrity of mitochondria. In physiologically‐matured embryos (dehydration‐tolerant), mitochondria showed lower metabolism levels, and no decline in ROS scavenging enzyme activities and less accumulation of thiobarbituric acid‐reactive products after embryo dehydration. These data indicate that seed desiccation‐tolerance acquisition might be associated with down‐adjustment of the metabolism level in the late development stage, resulting in less ROS production, and ROS scavenging enzymes becoming desiccation‐tolerant and then ensuring the structure and functional integrity of mitochondria.

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