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pubmed:abstractText |
Newly synthesized DNA is rapidly assembled into mature nucleosomes by the deposition of pre-existing and nascent histones, and some parts of this process are facilitated by chromatin assembly factor 1 (CAF-1). Loss-of-function mutants of CAF-1 in Arabidopsis, fasciata (fas), show a variety of morphological abnormalities and unique defects in gene expression in the meristems. In order to clarify the implications of CAF-1 in the maintenance of chromatin states in higher eukaryotes, we investigated transcriptional gene silencing (TGS) of various genes in fas mutants. Here, we show that TGS of endogenous CACTA transposons was released in a stochastic manner in fas. Other endogenous silent genes, a transposon AtMu1 and a hypothetical gene T5L23.26 at a heterochromatin knob, were also transcriptionally activated, and the activation of the three different silent loci at different chromosomal sites occurred non-concomitantly with each other. Furthermore, TGS of the silent beta-glucuronidase (GUS) transgene was also de-repressed randomly in fas. We conclude that CAF-1 ensures the stable inheritance of epigenetic states through growth and development in Arabidopsis.
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