Polycomb group proteins function in the female gametophyte to determine seed development in plants

Abstract

Polycomb group (PcG) proteins are evolutionary conserved proteins that stably maintain established transcriptional patterns over cell generations. The FERTILIZATION INDEPENDENT SEED (FIS) PcG complex from plants has a similar composition to the Polycomb repressive complex 2 from animals. Mutations in FIS genes cause parent-of-origin-dependent seed abortion. Every seed inheriting a mutant fis allele from the mother is destined to abort, regardless of the presence of a wild-type paternal allele. We tested in Arabidopsis whether the parent-of-origin-dependent seed abortion caused by lack of the FIS subunit MSI1 is caused by parental imprinting of the MSI1 gene. Our data show that MSI1 is not an imprinted gene and that early paternal MSI1 expression is not sufficient to rescue msi1 mutant seeds. By contrast, expression of MSI1 in msi1 female gametophytes is necessary to restore normal seed development, strongly arguing that the female gametophytic effect of fis mutants is caused by a functional requirement for an intact FIS complex in the female gametophyte. Thus, FIS-mediated expression patterns established in the female gametophyte can impact on seed development, establishing fis mutants as true female gametophytic maternal-effect mutants.

Sperm entry is sufficient to trigger division of the central cell but the paternal genome is required for endosperm development in Arabidopsis

“…However mechanisms causing zygotic activation and controlling karyogamy remain unknown and might differ between fertilization of the egg cell and fertilization of the central cell. With a few exceptions (Bayer et al, 2009;Leroy et al, 2007;Springer et al, 2000), the importance of parentally inherited transcripts has not been established and when the onset of transcription and translation takes place is unclear (Meyer and Scholten, 2007;Vielle-Calzada et al, 2000;Weijers et al, 2001). A global delay of paternal genome expression is expected to make early seed development independent from the presence of the paternal genome.…”

Genomic Imprinting Was Evolutionarily Conserved during Wheat Polyploidization

“…This finding suggests that MEA and FIS2 restrain seed growth (Chaudhury et al, 1997;Grossniklaus et al, 1998;Kiyosue et al, 1999;Luo et al, 1999). However, other studies have argued that the expression level rather than the imprinting pattern of a gene is likely indispensable for phenotypic variation, as plants with loss of function of MULTICOPY SUPPRESSOR OF IRA1, which encodes a nonimprinted subunit of PRC2, exhibit the same phenotypes as those with mutations in MEA and FIS2 (Köhler et al, 2003;Guitton and Berger, 2005;Leroy et al, 2007). In addition, emerging evidence suggests that paternally expressed genes are involved in establishing postzygotic hybridization barriers in A. thaliana, as downregulating the expression of the paternally imprinted genes ADMETOS, SU(VAR)3-9, HOMOLOG7, PATERNALLY EXPRESSED IMPRINTED GENE2 (PEG2), and PEG9 can partially rescue triploid seed development (Kradolfer et al, 2013;Wolff et al, 2015).…”

Cloning and Sequence Analysis of Apomixis Related Gene MSI1 (Multicopy Suppressor of Ira1) in Taraxacum antungense

“…Obviously, this result is similar to apomixis (Kohler and Makarevich, 2006). The male source alleles of MEA and FIS2 could be printed, but the MSI1 is not male source print (Leroy et al, 2007). The mutant MSI1 can develop seeds with diploid endosperm which does not need pollination, but this may hinder the development of embryo at an early stage.…”