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Dosage-dependent deregulation of an AGAMOUS-LIKE gene cluster contributes to interspecific incompatibility.

ABSTRACT: Postzygotic lethality of interspecies hybrids can result from differences in gene expression, copy number, or coding sequence and can be overcome by altering parental genome dosage. In crosses between Arabidopsis thaliana and A. arenosa, embryo arrest is associated with endosperm hyperproliferation and delayed development similar to paternal-excess interploidy crosses and polycomb-repressive complex (PRC) mutants. Failure is accompanied by parent-specific loss of gene silencing including the dysregulation of three genes suppressed by PRC. Increasing the maternal genome dosage rescues seed development and gene silencing. A gene set upregulated in the failing seed transcriptome encoded putative AGAMOUS-LIKE MADS domain transcription factors (AGL) that were expressed in normal early endosperm and were shown to interact in a previous yeast 2-hybrid analysis. Suppression of these AGL's expression upon cellularization required PRC. Preceding seed failure, expression of the PRC member FIS2 decreased concomitant with overexpression of the AGL cluster. Inactivating two members, AGL62 and AGL90, attenuated the postzygotic barrier between A. thaliana and A. arenosa. We present a model where dosage-sensitive loss of PRC function results in a dysregulated AGL network, which is detrimental for early seed development.

SUBMITTER: Walia H

PROVIDER: S-EPMC6754343 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature

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Dosage-dependent deregulation of an AGAMOUS-LIKE gene cluster contributes to interspecific incompatibility.

Walia Harkamal H Josefsson Caroline C Dilkes Brian B Kirkbride Ryan R Harada John J Comai Luca L

Current biology : CB 20090625 13

Postzygotic lethality of interspecies hybrids can result from differences in gene expression, copy number, or coding sequence and can be overcome by altering parental genome dosage. In crosses between Arabidopsis thaliana and A. arenosa, embryo arrest is associated with endosperm hyperproliferation and delayed development similar to paternal-excess interploidy crosses and polycomb-repressive complex (PRC) mutants. Failure is accompanied by parent-specific loss of gene silencing including the dys ...[more]

PMID: 19559614

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Project description:The cohesin complex plays critical roles in genomic stability and gene expression through effects on 3D architecture. Cohesin core subunit genes are mutated across a wide cross-section of cancers, but not in germinal center (GC) derived lymphomas. In spite of this, haploinsufficiency of cohesin ATPase subunit Smc3 was shown to contribute to malignant transformation of GC B-cells in mice. Herein we explored potential mechanisms and clinical relevance of Smc3 deficiency in GC lymphomagenesis. Transcriptional profiling of Smc3 haploinsufficient murine lymphomas revealed downregulation of genes repressed by loss of epigenetic tumor suppressors Tet2 and Kmt2d. Profiling 3D chromosomal interactions in lymphomas revealed impaired enhancer-promoter interactions affecting genes like Tet2, which was aberrantly downregulated in Smc3 deficient lymphomas. Tet2 plays important roles in B-cell exit from the GC reaction, and single cell RNA-seq profiles and phenotypic trajectory analysis in Smc3 mutant mice revealed a specific defect in commitment to the final steps of plasma cell differentiation. Although Smc3 deficiency resulted in structural abnormalities in GC B-cells, there was no increase of somatic mutations or structural variants in Smc3 haploinsufficient lymphomas, suggesting that cohesin deficiency largely induces lymphomas through disruption of enhancer-promoter interactions of terminal differentiation and tumor suppressor genes. Strikingly, the presence of the Smc3 haploinsufficient GC B-cell transcriptional signature in human patients with GC-derived diffuse large B-cell lymphoma (DLBCL) was linked to inferior clinical outcome and low expression of cohesin core subunits. Reciprocally, reduced expression of cohesin subunits was an independent risk factor for worse survival int DLBCL patient cohorts. Collectively, the data suggest that Smc3 functions as a bona fide tumor suppressor for lymphomas through non-genetic mechanisms, and drives disease by disrupting the commitment of GC B-cells to the plasma cell fate.

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Dosage-dependent deregulation of an AGAMOUS-LIKE gene cluster contributes to interspecific incompatibility.

Publications

Dosage-dependent deregulation of an AGAMOUS-LIKE gene cluster contributes to interspecific incompatibility.

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