DNA methylation and the promotion of flowering by vernalization

Abstract

We have tested the hypothesis that the promotion of flowering by prolonged exposure to low temperatures Many plants growing at high latitudes require exposure, as germinating seeds or vegetatively growing plants, to prolonged periods at low temperatures (vernalization) before they will initiate flowering. This ensures that flowering will occur in the warm days of spring and summer, which are favorable for pollination and seed development. Whereas some plants have an absolute requirement for vernalization, others, such as the late-flowering ecotypes of Arabidopsis, show a facultative requirement for vernalization, and will eventually flower even in the absence of a cold treatment (for review see ref. 1). The phenomenon of vernalization was first described in the middle of the 19th century (Kleppart, cited in ref.2), but only recently has a hypothesis suggesting a molecular mechanism for the low-temperature promotion of flowering been proposed (3).The cold treatment is perceived by cells, mitotically active at the time of treatment; early flowering results when these cells, or their descendants, form the floral͞inflorescence meristem, indicating that the vernalization signal is inherited mitotically rather than being transmitted from ''vernalized cells'' to the apex (4, 5). The vernalization signal is not transmitted to sexual progeny (1). The perceived parallels between the inheritance of the vernalization signal and of DNA methylation patterns led to the hypothesis that the vernalization response, in Arabidopsis and other plants, is mediated by changes in DNA methylation (3). Specifically it was proposed that the cold treatment results in demethylation of the promoter region(s) and subsequent activation of a gene or genes critical for initiating reproductive development. Mitotic inheritance of the vernalization signal is consistent with clonal inheritance of DNA methylation patterns (6), but it is now known that, in plants, methylation patterns may not be reset between generations (7-9), suggesting that factors other than DNA methylation may be involved in resetting the vernalization signal.Treatment of plants with the demethylating agent, 5-azacytidine (5-azaC) resulted in early flowering (3, 10). This earlyflowering response was restricted to plants that normally respond to vernalization, including certain late-flowering ecotypes and mutants of Arabidopsis and winter wheat. Spring wheats and other late-flowering Arabidopsis mutants that are insensitive to vernalization did not develop an early-flowering phenotype after 5-azaC treatment. These observations suggest that this response was specific to the vernalization-dependent pathway to flowering (3, 10, 11) rather than being a nonspecific effect of the treatment.In addition to causing demethylation, 5-azaC is a general inhibitor of transcription (12), so it is possible that the promotion of flowering by 5-azaC resulted from effects other than demethylation of DNA. To discriminate between these possibilities we have used Arabidopsis plants in which meth...

Flowering induced by 5‐azacytidine, a DNA demethylating reagent in a short‐day plant, Perilla frutescens var. crispa

“…This means that the present experimental system may be useful to study the regulation mechanism of the flowering-related genes in P. frutescens. After the start of 5-azacytidine treatment Comparison of flowering induced by 5-azacytidine and that induced by SD 5-Azacytidine effectively induced flowering even when applied to the shoot apical meristem of P. frutescens seedlings (Table 4) as compared with the previous works in which 5-azacytidine was treated to seeds (Sano et al 1990, Burn et al 1993, Brock and Davidson 1994, Finnegan et al 1998a, Demeulemeester et al 1999. As reported by Zeevaart (1958), P. frutescens seedlings respond to SD treatment only after the fourth leaf pair expanded.…”

“…antisense-methyltransferase cDNA (MET1) induced flowering and downregulation of FLC expression in A. thaliana (Finnegan et al 1998a, Sheldon et al 1999. These results indicate that the flowering genes are upregulated through the decrease in DNA methylation Amasino 2000, 2001).…”

Is DNA methylation modulated by wounding-induced oxidative burst in maize?

“…A physiological effect of DNA methylation was shown by treatment of germinated rice seeds with 5-azadeoxycitidine, a powerful demethylation agent, which induced dwarfism at maturity (Sano et al, 1990). Finnegan et al (1998) One hour after wounding of maize leaves two methylcytosines in positions 100 and 126 located in a CpG island overlapping the first exon of the ZmCPK11 gene are demethylated, and 3-6 h after wounding the transcript level of the kinase is markedly increased (Szczegielniak et al, 2005). This suggests that reversible methylation of cytosines 100 and 126 is involved in the regulation of ZmCPK11 transcription under stress, in accord with the general opinion that cytosine demethylation results in activation of transcription (Zhang et al, 2006;Zilberman et al, 2007).…”

“…Hypermethylation of DNA usually decreases gene expression, while reduction of the methylation level (hypomethylation) leads to higher gene expression (Finnegan et al, 1998).…”

The Suppressor‐mutator element and the evolutionary riddle of transposons

“…Today it is increasingly evident that epigenetic mechanisms are central to the developmental regulation of certain genes in both plants and animals. Chromatin complexes formed by the Polycomb Group of genes in Drosophila, the stable inactivation of imprinted genes in mammals, and the methylation of vernalization and flowering genes in plants, are all examples of contemporary epigenetic developmental regulatory mechanisms (Finnegan et al 1996;Jaenisch 1997;Pirrotta 1997;Richards 1997;Finnegan et al 1998). The underlying molecular mechanisms are just now being elucidated.…”