The gametophytic maternal effect mutant medea (mea) shows aberrant growth regulation during embryogenesis in Arabidopsis thaliana. Embryos derived from mea eggs grow excessively and die during seed desiccation. Embryo lethality is independent of the paternal contribution and gene dosage. The mea phenotype is consistent with the parental conflict theory for the evolution of parent-of-origin-specific effects. MEA encodes a SET domain protein similar to Enhancer of zeste, a member of the Polycomb group. In animals, Polycomb group proteins ensure the stable inheritance of expression patterns through cell division and regulate the control of cell proliferation.

In higher plants, seed development requires maternal gene activity in the haploid (gametophytic) as well as diploid (sporophytic) tissues of the developing ovule. The Arabidopsis thaliana gene MEDEA (MEA) encodes a SET-domain protein of the Polycomb group that regulates cell proliferation by exerting a gametophytic maternal control during seed development. Seeds derived from female gametocytes (embryo sacs) carrying a mutant mea allele abort and exhibit cell proliferation defects in both the embryo and the endosperm. In this study we show that the mea mutation affects an imprinted gene expressed maternally in cells of the female gametophyte and after fertilization only from maternally inherited MEA alleles. Paternally inherited MEA alleles are transcriptionally silent in both the young embryo and endosperm. Mutations at the decrease in DNA methylation1 (ddm1) locus are able to rescue mea seeds by functionally reactivating paternally inherited MEA alleles during seed development. Rescued seeds are larger than the wild type and exhibit some of the abnormalities found in aborting mea seeds. Our results indicate that the maintenance of the genomic imprint at the mea locus requires zygotic DDM1 activity. Because DDM1 encodes a putative chromatin remodeling factor, chromatin structure is likely to be interrelated with genomic imprinting in Arabidopsis.

Isolation of cDNA clones for the mouse CCAAT binding factor (mCBF) has revealed the expression of two distinct forms of mCBF that are generated by alternative splicing of a single primary transcript from a gene that maps to chromosome 17. The mCBF1 mRNA encodes a protein of 997 amino acids, whereas the mCBF2 protein is predicted to be only 461 amino acids in length; mCBF1 and human CBF (hCBF) share>80% amino acid sequence identity. Analysis of adult mouse tissue RNAs has revealed that the mCBF1 and mCBF2 mRNAs are ubiquitously expressed, but that mCBF1 mRNA is 5- to 10-fold more abundant than mCBF2 mRNA. Similarly, mCBF mRNA was detected through-out the placenta and in all tissues of the developing embryo from day 8 to day 18 of gestation. Overexpression of the two forms of mCBF in mammalian cells has demonstrated that the mCBF1 and mCBF2 proteins localize to different cellular compartments, with mCBF1 found predominantly in the nucleus and mCBF2 restricted to the cytoplasm. Co-expression of these two forms influences their localization, however, indicating that CBF activity can be regulated by the relative amounts of the two forms expressed in a cell.