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Published February 15, 2000 | public
Journal Article

Ectopic hypermethylation of flower-specific genes in Arabidopsis

Abstract

Background: Arabidopsis mutations causing genome-wide hypomethylation are viable but display a number of specific developmental abnormalities, including some that resemble known floral homeotic mutations. We previously showed that one of the developmental abnormalities present in an antisense-METHYLTRANSFERASEI (METI) transgenic line resulted from ectopic hypermethylation of the SUPERMAN gene. Results: Here, we investigate the extent to which hypermethylation of SUPERMAN occurs in several hypomethylation mutants, and describe methylation effects at a second gene, AGAMOUS. SUPERMAN gene hypermethylation occurred at a high frequency in several mutants that cause overall decreases in genomic DNA methylation. The hypermethylation pattern was largely similar in the different mutant backgrounds. Genetic analysis suggests that hypermethylation most likely arose either during meiosis or somatically in small sectors of the plant. A second floral development gene, AGAMOUS, also became hypermethylated and silenced in an Arabidopsis antisense-METI line. Conclusions: These results suggest that ectopic hypermethylation of specific genes in mutant backgrounds that show overall decreases in methylation may be a widespread phenomenon that could explain many of the developmental defects seen in Arabidopsis methylation mutants. This resembles a phenomenon seen in cancer cells, which can simultaneously show genome-wide hypomethylation and hypermethylation of specific genes. Comparison of the methylated sequences in SUPERMAN and AGAMOUS suggests that hypermethylation could involve DNA secondary structures formed by pyrimidine-rich sequences.

Additional Information

© 2000 Elsevier Science Ltd. Received: 22 October 1999. Revised: 17 December 1999. Accepted: 17 December 1999. Published: 4 February 2000. We thank Eric Richards for providing seeds of the ddm1-2 and ddm2-1 mutants, Jurek Paszkowski and Ortrun Mittelsten Scheid for seeds of the som mutants, and Steve Smith and Juli Feigon for helpful discussions. This work was supported by California Division — American Cancer Society Fellowship #1-14-98 and a Jonsson Cancer Center Foundation/UCLA seed grant ACS #IRG 78-001-21 (to S.E.J.) and NIH grant GM45697 and a W. M. Keck Foundation Grant for Basic Medical Research to (E.M.M.).

Additional details

Created:
August 21, 2023
Modified:
October 23, 2023