Abstract
As the last stage of leaf development, senescence is a fine-tuned process regulated by interplays of multiple signaling pathways. We have previously identified soybean (Glycine max) SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE (SARK), a leucine-rich repeat-receptor-like protein kinase from soybean, as a positive regulator of leaf senescence. Here, we report the elucidation of the molecular mechanism of GmSARK-mediated leaf senescence, especially its specific roles in senescence-inducing hormonal pathways. A glucocorticoid-inducible transcription system was used to produce transgenic Arabidopsis (Arabidopsis thaliana) plants for inducible overexpression of GmSARK, which led to early leaf senescence, chloroplast destruction, and abnormal flower morphology in Arabidopsis. Transcript analyses of the GmSARK-overexpressing seedlings revealed a multitude of changes in phytohormone synthesis and signaling, specifically the repression of cytokinin functions and the induction of auxin and ethylene pathways. Inhibition of either auxin action or ethylene biosynthesis alleviated the senescence induced by GmSARK. Consistently, mutation of either AUXIN RESISTANT1 or ETHYLENE INSENSITIVE2 completely reversed the GmSARK-induced senescence. We further identified a homolog of GmSARK with a similar expression pattern in Arabidopsis and named it AtSARK. Inducible overexpression of AtSARK caused precocious senescence and abnormal floral organ development nearly identical to the GmSARK-overexpressing plants, whereas a T-DNA insertion mutant of AtSARK showed significantly delayed senescence. A kinase assay on recombinant catalytic domains of GmSARK and AtSARK revealed that these two leucine-rich repeat-receptor-like protein kinases autophosphorylate on both serine/threonine and tyrosine residues. We inferred that the SARK-mediated pathway may be a widespread mechanism in regulating leaf senescence.
Highlights
As the last stage of leaf development, senescence is a fine-tuned process regulated by interplays of multiple signaling pathways
Semiquantitative reverse transcription (RT)-PCR analysis showed that the 24-h DEX treatment induced high expression levels of GmSARK in lines S9, S23, and S33, whereas the transcript of GmSARK was undetectable in the S48 and G28 seedlings (Fig. 1Ac), indicating that the expression of GmSARK was silenced in line S48
We have previously demonstrated, using GmSARKRNAi and 35S:GmSARK transgenic plants, that GmSARK plays a critical role in the regulation of soybean leaf senescence (Li et al, 2006)
Summary
As the last stage of leaf development, senescence is a fine-tuned process regulated by interplays of multiple signaling pathways. Several transcription factors, including NAC1, AtNAC2, AtNAP, WRKY6, WRKY53, RAV1, and CBF2, have been demonstrated to play important roles in the regulation of leaf senescence (Robatzek and Somssich, 2002; Miao et al, 2004; Guo and Gan, 2006; Kim et al, 2009; Sharabi-Schwager et al, 2010). Despite these impressive advances in the field, the nature of the plant developmental age, the transduction pathway of the so-called senescence signal, and the mechanisms of action of and the interactions between exogenous and endogenous regulatory factors during this process have not been fully defined. There is evidence that AHK3 and ARR2 are negative regulators of leaf senescence, the specific molecular mechanisms involved in their regulation of this process remain unknown
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