AtWAKL10, a Cell Wall Associated Receptor-Like Kinase, Negatively Regulates Leaf Senescence in Arabidopsis thaliana.

Lu Li,Yongfeng Guo,Akhtar Ali,Kui Li

doi:10.3390/ijms22094885

Abstract

Receptor-like kinases (RLKs) constitute a large group of cell surface receptors that play crucial roles in multiple biological processes. However, the function of most RLKs in plants has not been extensively explored, and much less for the class of cell wall associated kinases (WAKs) and WAK-like kinases (WAKLs). In this study, analyses of developmental expression patterns uncovered a putative role of AtWAKL10 in modulating leaf senescence, which was further investigated at physiological and molecular levels. The expression level of AtWAKL10 increased with the developmental progression and was rapidly upregulated in senescing leaf tissues. The promoter of AtWAKL10 contains various defense and hormone responsive elements, and its expression could be significantly induced by exogenous ABA, JA and SA. Moreover, the loss-of-function atwakl10 mutant showed earlier senescence along the course of natural development and accelerated leaf senescence under darkness and hormonal stresses, while plants overexpressing AtWAKL10 showed an opposite trend. Additionally, some defense and senescence related WRKY transcription factors could bind to the promoter of AtWAKL10. In addition, deletion and overexpression of AtWAKL10 caused several specific transcriptional alterations, including genes involved in cell extension, cell wall modification, defense response and senescence related WRKYs, which may be implicated in regulatory mechanisms adopted by AtWAKL10 in controlling leaf senescence. Taken together, these results revealed that AtWAKL10 negatively regulated leaf senescence.

Highlights

Leaf development is a strictly programmed process that includes the early stages of leaf development such as initiation, growth, and maturation, and the later leaf senescence.Due to the sessile lifestyle of plants, leaf senescence is regulated by intrinsic and genetic factors, and affected by various environmental stimuli, such as drought, shade, extreme temperature, and pathogen infections [1,2]
Functional domains along the AtWAKL10 protein sequence were identified through the SMART v9 service program and a signal peptide of 24 aa with a likelihood of 0.991 as well as the corresponding cleavage site at Ala24-Ser25 were predicted by using the SignalP-5.0 program (Figure 1A)
We functionally characterized the Arabidopsis cell wall associated receptor-like kinase AtWAKL10, which exhibited the highest expression levels in naturally senescing leaves

Summary

Introduction

Leaf development is a strictly programmed process that includes the early stages of leaf development such as initiation, growth, and maturation, and the later leaf senescence.Due to the sessile lifestyle of plants, leaf senescence is regulated by intrinsic and genetic factors, and affected by various environmental stimuli, such as drought, shade, extreme temperature, and pathogen infections [1,2]. Leaf development is a strictly programmed process that includes the early stages of leaf development such as initiation, growth, and maturation, and the later leaf senescence. Leaf senescence is a complicated multi-step process. In contrast to nutrient assimilation at early development stages, leaf senescence is mainly accompanied by highly ordered degradation of organelles and cellular compositions, subsequent remobilization of valuable resources from senescing leaves to vigorous tissues and organs, and eventually, the suspension of photosynthesis and programmed cell death [3,4,5]. Following the initiation of leaf senescence, leaves will experience constant chlorophyll loss, reduced efficiency of photosynthesis, and increased accumulation of reactive oxygen species (ROS) [5,6,7]. To cope with the substantial metabolic loss during leaf senescence, plants have established sophisticated transcriptional regulatory networks and signaling mechanisms to support plant growth and ensure reproduction by stimulating the expression of senescence associated genes (SAGs) [2,8,9]

Methods

Results

Discussion

Conclusion