Abstract

Premature leaf senescence occurs in the ultimate phase of the plant, and it occurs through a complex series of actions regulated by stress, hormones and genes. In this study, a proteomic analysis was performed to analyze the factors that could induce premature leaf senescence in two cotton cultivars. We successfully identified 443 differential abundant proteins (DAPs) from 7388 high-confidence proteins at four stages between non-premature senescence (NS) and premature senescence (PS), among which 158 proteins were over-accumulated, 238 proteins were down-accumulated at four stages, and 47 proteins displayed overlapped accumulation. All the DAPs were mapped onto 21 different categories on the basis of a Clusters of Orthologous Groups (COG) analysis, and 9 clusters were based on accumulation. Gene Ontology (GO) enrichment results show that processes related to stress responses, including responses to cold temperatures and responses to hormones, are significantly differentially accumulated. More importantly, the enriched proteins were mapped in The Arabidopsis Information Resource (TAIR), showing that 58 proteins play an active role in abiotic stress, hormone signaling and leaf senescence. Among these proteins, 26 cold-responsive proteins (CRPs) are significantly differentially accumulated. The meteorological data showed that the median temperatures declined at approximately 15 days before the onset of aging, suggesting that a decrease in temperature is tightly linked to an onset of cotton leaf senescence. Because accumulations of H2O2 and increased jasmonic acid (JA) were detected during PS, we speculate that two pathways associated with JA and H2O2 are closely related to premature leaf senescence in cotton.

Highlights

  • Leaf senescence is an important physiological phenomenon that is defined as an age-dependent progression in the plant’s ultimate phase that leads to death or occurs at the end of the life span [1]

  • Our results indicated that the onset of cotton premature leaf senescence is tightly linked to a decrease in temperature, and two pathways associated with hydrogen peroxide, jasmonic acid (JA) biosynthesis, and signaling are key factors in shaping cold-induced cotton leaf senescence

  • Gene Ontology (GO) enrichment analysis showed that differential abundant proteins (DAPs) associated with abiotic stress, and especially those responding to cold temperatures, are differentially accumulated during the four stages

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Summary

Introduction

Leaf senescence is an important physiological phenomenon that is defined as an age-dependent progression in the plant’s ultimate phase that leads to death or occurs at the end of the life span [1]. Colder temperatures (20 ◦C or less) serve as a key predisposing factor, and they contribute to premature leaf senescence These temperatures can increase the malondialdehyde (MDA) content and decrease the soluble protein and chlorophyll contents, resulting in the inhibition of vegetative growth and decreased net photosynthesis [4,5,6]. They can lead to accelerated senescence of part of the leaf surface by reducing the lifespan of the photosynthetic machinery and the leaf lifetime carbon gain [7]. Plant hormones, endogenous factors (abscisic acid (ABA), cytokinin (CK) and ethylene (ET) [1,11,12,13] and other environmental factors (drought [14], salinity [15] and nutrient deficiency [16]) play key roles in senescence regulation

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