Abstract

A cold night can follow a hot day, and because they cannot move, plants subjected to such temperature fluctuations must acclimate on the basis mainly of pre-existing proteins. Zhang et al. report in a paper in BMC Plant Biology, however, that heat-induced cell death results from transcriptional activation of a kinase related to disease resistance factors and leading to a localized hypersensitive response. This specialized response reflects the failure of adaptations that normally enable plants to survive over a remarkable temperature range, by mechanisms that are not fully understood.

Highlights

  • A cold night can follow a hot day, and because they cannot move, plants subjected to such temperature fluctuations must acclimate on the basis mainly of preexisting proteins

  • To state it another way, mammalian enzymes and constituent processes fail outside a narrow window of optimal temperatures, and such failure is catastrophic for the organism, whereas plants can maintain and coordinate cellular processes over a broad temperature range

  • When coordination between key cellular processes fails, cell death can result. This can occur in plant cells as part of a localized hypersensitive response to pathogen attack, a strategy to restrict the growth of the invader

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Summary

Introduction

A cold night can follow a hot day, and because they cannot move, plants subjected to such temperature fluctuations must acclimate on the basis mainly of preexisting proteins. Exceeding the homeostatic limits for managing reactive oxygen species at high temperature results in localized cell death. To state it another way, mammalian enzymes and constituent processes fail outside a narrow window of optimal temperatures, and such failure is catastrophic for the organism, whereas plants can maintain and coordinate cellular processes over a broad temperature range.

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