Search

Leaf senescence is a complex but tightly regulated developmental process involving a coordinated sequence of multiple molecular events, which ultimately leads to death of the leaf. Efforts to understand the mechanistic principles underlying leaf senescence have been largely made by transcriptomic, proteomic, and metabolomic studies over the past decade. This review focuses on recent milestones in leaf senescence research obtained using multi-omics technologies, as well as future endeavors toward systems understanding of leaf senescence processes. In particular, we discuss recent advances in understanding molecular events during leaf senescence through genome-wide transcriptome analyses in Arabidopsis . We also describe comparative transcriptome analyses used to unveil the commonality and diversity of regulatory mechanisms governing leaf senescence in the plant kingdom. Finally, we provide current illustrations of epigenomic, proteomic, and metabolomic landscapes of leaf senescence. We envisage that integration of multi-omics leaf senescence data will enable us to address unresolved questions regarding leaf senescence, including determining the molecular principles that coordinate concurrent and ordered changes in biological events during leaf senescence. [ABSTRACT FROM AUTHOR]

Methylcytosine-binding proteins containing SRA (SET- and RING-Associated) domain are required for the establishment and/or maintenance of DNA methylation in both plants and animals. We previously proposed that Arabidopsis VIM/ORTH proteins with an SRA domain maintain DNA methylation and epigenetic gene silencing in heterochromatic regions. However, their endogenous targets of epigenetic gene silencing have not been analyzed globally and the mechanisms by which VIM proteins coordinate DNA methylation and epigenetic silencing are largely unknown. In this study, a genome-wide transcript profiling analysis revealed 544 derepressed genes in a vim1/2/3 triple mutant, including 133 known genes. VIM1 bound to promoter and transcribed regions of the up-regulated genes in vim1/2/3 and VIM deficiency caused severe DNA hypomethylation in all sequence contexts at direct VIM1 targets. We found a drastic loss of H3K9me2 at heterochromatic chromocenters in vim1/2/3 nuclei. Furthermore, aberrant changes in transcriptionally active and repressive histone modifications were observed at VIM1 targets in vim1/2/3. VIM1-binding capacity to target genes was significantly reduced in the met1 background, indicating that VIM1 primarily recognizes CG methylation deposited by MET1. Overall, our data indicate that VIM proteins regulate genome-wide epigenetic gene silencing through coordinated modulation of DNA methylation and histone modification status in collaboration with MET1., (© The Author 2014. Published by the Molecular Plant Shanghai Editorial Office in association with Oxford University Press on behalf of CSPB and IPPE, SIBS, CAS.)