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Leaf senescence is a finely regulated complex process; however, evidence for the involvement of epigenetic processes in the regulation of leaf senescence is still fragmentary. Therefore, we chose to examine the functions of DRD1, a SWI2/SNF2 chromatin remodeling protein, in epigenetic regulation of leaf senescence, particularly because drd1-6 mutants exhibited a delayed leaf senescence phenotype. Photosynthetic parameters such as Fv/Fm and ETRmax were decreased in WT leaves compared to leaves of drd1-6 mutants after dark treatment. The WT leaves remarkably lost more chlorophyll and protein content during dark-induced senescence (DIS) than the drd1-6 leaves did. The induction of senescence-associated genes was noticeably inhibited in the drd1-6 mutant after 5-d of DIS. We compared changes in epigenetic regulation during DIS via quantitative expression analysis of 180-bp centromeric ( CEN) and transcriptionally silent information ( TSI) repeats.

Their expression levels significantly increased in both the WT and the drd1-6 mutant, but did much less in the latter. Moreover, the delayed leaf senescence was observed in ddm1-2 mutants as well as the drd1-6, but not in drd1-p mutants. These data suggest that SWI2/SNF2 chromatin remodeling proteins such as DRD1 and DDM1 may influence leaf senescence possibly via epigenetic regulation. Introduction Leaf senescence is an endogenously controlled degenerative process that occurs in the final stage of leaf development, leading to leaf death [, ]. During leaf senescence, a series of events involving the degradation of chloroplast, decrease in photosynthetic activity, loss of chlorophyll, and the recycling of valuable nutrients to other parts of the plant, occur []. Initial chloroplast degradation is followed by nuclear and vacuolar breakdown. This latter mechanism is accompanied by the release of nucleases and proteases, acidification of the cytoplasm, and rapid degradation of nucleic acids and proteins [, ].

Developmental senescence is a highly regulated genetic process that occurs in an age-dependent manner []; however, it is also influenced by complex interaction of developmental stage with various internal and external factors []. Internal factors include developmental age, diverse phytohormones, and reproductive development. External or environmental factors include stresses such as high light intensity, temperature extremes, drought, ozone, shading, nutrient deficiency, and pathogen infection.

It is clear that multiple pathways regulating multiple internal and external factors exist and are interconnected to form a complex network that regulates senescence. Studies of changes in gene expression by using microarray analysis have shown that senescence is often regulated by transcription factors. Over 800 genes have been identified as senescence-associated genes (SAGs), and among them, over 100 genes encode transcription factors [, ], including WRKY, NAC, MYB, TUB, bZIP, and C2H2 transcription factor families. The Arabidopsis WRKY53 transcription factor plays a central role in the regulation of the early stages of senescence [–]. A knock-out line of the WRKY53 gene shows delayed leaf senescence; on the other hand, overexpression of this gene leads to precocious senescence [, ].

The WRKY53 transcription factor controls several SAGs involved in the control of leaf senescence []. Epigenetic regulation plays an important role in cellular senescence and organism aging in higher organisms [–]. The epigenetic mechanisms including DNA methylation, histone modification, and ATP-dependent chromatin remodeling control expression of the senescence-associated genes ( SAGs) by reprogramming of chromatin state with aging. Interestingly, global DNA hypomethylation and specific loci hypermethylation occur in aging.

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Recently, many molecules that control global alteration in chromatin structure during senescence have been analyzed. Screening of activation-tagged lines in Arabidopsis for delayed leaf senescence identified the ORE7/ESC gene, which encodes an AT-hook DNA-binding protein. Expression of ORE7 results in a dosage-dependent effect on the initiation of leaf senescence and interphase chromatin organization []. It was also reported that histones at the WRKY53 promoter and coding regions undergo H3K4 methylation to be active chromatin state for upregulation of target SAGs after onset of leaf senescence []. However, in case of the SWITCH/ SUCROSE NONFERMENTING (SWI/SNF) chromatin remodelers, its role in leaf senescence has not been explored in spite of existence of a number of SWI/SNF chromatin remodelers.