UBIQUITIN-SPECIFIC PROTEASE 26 Is Required for Seed Development and the Repression of PHERES1 in Arabidopsis

Abstract

The Arabidopsis mutant Atubp26 initiates autonomous endosperm at a frequency of $1% in the absence of fertilization and develops arrested seeds at a frequency of $65% when self-pollinated. These phenotypes are similar to those of the FERTILIZATION INDEPENDENT SEED (FIS) class mutants, mea, fis2, fie, and Atmsi1, which also show development of the central cell into endosperm in the absence of fertilization and arrest of the embryo following fertilization. Atubp26 results from a T-DNA insertion in the UBIQUITIN-SPECIFIC PROTEASE gene AtUBP26, which catalyzes deubiquitination of histone H2B and is required for heterochromatin silencing. The paternal copy of AtUBP26 is able to complement the loss of function of the maternal copy in postfertilization seed development. This contrasts to the fis class mutants where the paternal FIS copy does not rescue aborted seeds. As in the fis class mutants, the Polycomb group (PcG) complex target gene PHERES1 (PHE1) is expressed at higher levels in Atubp26 ovules than in wild type; there is a lower level of H3K27me3 at the PHE1 locus. The phenotypes suggest that AtUBP26 is required for normal seed development and the repression of PHE1.

Involvement of KDM1C histone demethylase–OTLD1 otubain-like histone deubiquitinase complexes in plant gene repression

“…Mutations in Arabidopsis H2B deubiquitinase UBP26/ SUP32, which appears to be vital for heterochromatin formation, release heterochromatic silencing of transgenes and transposons (20). Also, a T-DNA insertion resulting in UBP26/SUP32 loss-of-function leads to up-regulation of PHE1, a MADS-box gene expressed in developing siliques (26). Another Arabidopsis ubiquitin-specific protease, UBP14, which may be directly involved in the ubiquitin/26S proteasome pathway, is essential for embryonic development (27).…”

Dynamic regulation of Polycomb group activity during plant development

“…A few other factors have been proposed to associate with PRC2 and to affect the catalysis of H3K27me3. These include AtUBP26, which probably deubiquitinates H2B at certain PRC2 target loci in the seed to enable trimethylation of H3K27 [44], and the plant-specific protein BLISTER (BLI), which interacts with CLF and represses a subset of PcG target genes [45].…”

Flickin’ the ubiquitin switch

“…Ubiquitylation and deubiquitylation of H2B are important at multiple stages of development in Arabidopsis. 16,[41][42][43][44][45][46][47] Mutations in the plant orthologues of dBre1, HUB1 and HUB2, cause a reduction in seed dormancy and plant size, as well as other pleiotropic phenotypes. 16,42 Four independent studies later found that mutant alleles of hub1 and hub2 give rise to an early-flowering phenotype.…”

“…53 Conversely, a mutation in ubp26 in a different genetic background was found to result in upregulation of the transcription factor-encoding PHE1 gene, with an associated reduction of H3K27me3 at this gene locus. 47 PHE1 is an example of paternal imprinting in Arabidopsis; the maternal allele is silenced by the FIS complex (the plant equivalent of the fly Polycomb Group complex) prior to fertilization, through tri-methylation of H3K27. 54 Luo et al 47 thus suggested that deubiquitylation of H2B by UBP26 may be a prerequisite for such H3K27 tri-methylation, in agreement with the finding that RNAi depletion of the H2B ubiquitin protease USP7 in fly S2 cell culture results in a global decrease of H3K27me3.…”

“…47 PHE1 is an example of paternal imprinting in Arabidopsis; the maternal allele is silenced by the FIS complex (the plant equivalent of the fly Polycomb Group complex) prior to fertilization, through tri-methylation of H3K27. 54 Luo et al 47 thus suggested that deubiquitylation of H2B by UBP26 may be a prerequisite for such H3K27 tri-methylation, in agreement with the finding that RNAi depletion of the H2B ubiquitin protease USP7 in fly S2 cell culture results in a global decrease of H3K27me3. 38,47 The disparate effects of UBP26 in two different genetic backgrounds (being required for either FLC transcription or PHE1 repression) hint at complex, gene differential effects and emphasize the redundancy of H2B ubiquitin proteases in higher eukaryotes, highlighting a need to confirm findings in reduced systems.…”