https://www.d.umn.edu/biology/documents/Winkler1.pdf

The Evolutionary Consequences of Polyploidy

Polycomb group complexes, which are known to regulate homeotic genes, have now been found to control hundreds of other genes in mammals and insects. First believed to progressively assemble and package chromatin, they are now thought to be localized, but induce a methylation mark on histone H3 over a broad chromatin domain. Recent progress has changed our view of how these complexes are recruited, and how they affect chromatin and repress gene activity. Polycomb complexes function as global enforcers of epigenetically repressed states, balanced by an antagonistic state that is mediated by Trithorax. These epigenetic states must be reprogrammed when cells become committed to differentiation.

Polycomb silencing mechanisms and the management of genomic programmes.

DNA methylation has two essential roles in plants and animals - defending the genome against transposons and regulating gene expression. Recent experiments in Arabidopsis thaliana have begun to address crucial questions about how DNA methylation is established and maintained. One cardinal insight has been the discovery that DNA methylation can be guided by small RNAs produced through RNA-interference pathways. Plants and mammals use a similar suite of DNA methyltransferases to propagate DNA methylation, but plants have also developed a glycosylase-based mechanism for removing DNA methylation, and there are hints that similar processes function in other organisms.

Gardening The Genome: DNA Methylation in Arabidopsis thaliana

During the mid-twentieth century Conrad Waddington proposed his ontogenic concept of canalization, and suggested that epigenetic mechanisms might serve as a means of metastable memory imposed on the genetic material during differentiation. Subsequently, Waddington's theories have received substantial acknowledgment during the first decade of the twenty-first century, with numerous studies unraveling the important contributions of epigenetic mechanisms and the epigenomic control of differentiation. The early embryogenesis and primordial germ cell development have received much attention as developmental stages with extensive epigenomic reprogramming. In both developmental phases, the epigenomic landscape of chromosomes is rapidly and dramatically altered, and this goes along with a substantial change in the developmental potential of cells. In this chapter, a summary is provided of the current knowledge of epigenetic reprogramming mechanisms. These are discussed in line with biological concepts, and with the role of DNA methylation in particular.


Keywords:

Zygote;
Chromatin;
Epigenome;
Genomic imprints;
Epigenetic reprogramming

Epigenetic Reprogramming in Mammalian Development

https://www.cell.com/cell/pdf/S0092-8674(02)00807-3.pdf

DEMETER, a DNA Glycosylase Domain Protein, Is Required for Endosperm Gene Imprinting and Seed Viability in Arabidopsis

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.

https://science.sciencemag.org/content/sci/280/5362/446.full.pdf

Maternal Control of Embryogenesis by MEDEA, a Polycomb Group Gene in Arabidopsis

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.

/pdf/maintenance-of-genomic-imprinting-at-the-arabidopsis-medea-34bxkhtpxy.pdf

Marilu A. Hoeppner

Papers

Maternal Control of Embryogenesis by MEDEA, a Polycomb Group Gene in Arabidopsis

Maintenance of genomic imprinting at the Arabidopsis medea locus requires zygotic DDM1 activity