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TRIM37 interacts with TRIM28 to maintain primordial germ cell identity during migration [bulkRNA-seq, scRNA-seq]

ABSTRACT: During embryo development, germ cells segregate from soma to ensure the genome transmission of a species. Although the repression of somatic programs in germline specification is well studied, the molecular mechanisms that protect primordial germ cell (PGC) fate thereafter remain poorly understood. Here, we show that the ubiquitin ligase TRIM37 suppresses the somatic programs during PGC migration. Trim37 mutant embryos exhibit PGC developmental defects from embryonic day 9.5 (E9.5) and depletion at E12.5, with Trim37-deficient PGCs transdifferentiating into somatic cells. Mechanistically, TRIM37 interacts with TRIM28 through its MATH domain to repress somatic gene expression in the nucleus. Forcing TRIM37 out of the nucleus causes PGC depletion. Additionally, the K27-linked polyubiquitination of TRIM28 catalyzed by TRIM37 augments their interaction and promotes the nucleus location of TRIM37. The impairment of TRIM37 ubiquitin ligase activity and mutations in TRIM28 ubiquitination sites both hinder PGC development. Furthermore, TRIM37 deficiency disrupts the DNA binding of TRIM28, which is mostly guided by AP2γ, leading to enhanced chromatin accessibility and increased H3K27ac levels, resulting in the upregulation of somatic genes. Our results shed light on the TRIM37-mediated epigenetic suppression mechanisms controlling germ cell fate maintenance and are relevant for the infertility of Mulibrey nanism patients.

ORGANISM(S): Mus musculus

PROVIDER: GSE289335 | GEO | 2026/06/26

REPOSITORIES: GEO

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TRIM37 interacts with TRIM28 to maintain primordial germ cell identity during migration

Project description:During embryo development, germ cells segregate from soma to ensure the genome transmission of a species. Although the repression of somatic programs in germline specification is well studied, the molecular mechanisms that protect primordial germ cell (PGC) fate thereafter remain poorly understood. Here, we show that the ubiquitin ligase TRIM37 suppresses the somatic programs during PGC migration. Trim37 mutant embryos exhibit PGC developmental defects from embryonic day 9.5 (E9.5) and depletion at E12.5, with Trim37-deficient PGCs transdifferentiating into somatic cells. Mechanistically, TRIM37 interacts with TRIM28 through its MATH domain to repress somatic gene expression in the nucleus. Forcing TRIM37 out of the nucleus causes PGC depletion. Additionally, the K27-linked polyubiquitination of TRIM28 catalyzed by TRIM37 augments their interaction and promotes the nucleus location of TRIM37. The impairment of TRIM37 ubiquitin ligase activity and mutations in TRIM28 ubiquitination sites both hinder PGC development. Furthermore, TRIM37 deficiency disrupts the DNA binding of TRIM28, which is mostly guided by AP2γ, leading to enhanced chromatin accessibility and increased H3K27ac levels, resulting in the upregulation of somatic genes. Our results shed light on the TRIM37-mediated epigenetic suppression mechanisms controlling germ cell fate maintenance and are relevant for the infertility of Mulibrey nanism patients.

2026-06-26 | GSE289334 | GEO

TRIM37 interacts with TRIM28 to maintain primordial germ cell identity during migration [ATAC-seq]

2026-06-26 | GSE289333 | GEO

TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene

Project description:The TRIM37 gene is mutatedin Mulbery nanism, a rare autosomal recessive disorder, and is in the 17q23 chromosomal region that is amplified in up to ~40% of breast cancers. Trim37 contains a RING finger domain, a hallmark of E3 ubiquitin ligases, but the protein substrate(s) of Trim37 is unknown. Mono-ubiquitination of histone H2A is a chromatin modification associated with transcriptional repression and here we report that Trim37 is an H2A ubiquitin ligase. Genome-wide Chip-CHIP experiments indicate that in human breast cancer cells containing amplified 17q23, Trim37 is bound to the promoters of many tumor suppressor genes. RNA interference (RNAi)-mediated knockdown of Trim37 results in loss of ubiquitinated H2A, dissociation of PRC1 and PRC2, and transcriptional reactivation of silenced genes. Knockdown of Trim37 in human breast cancer cells containing amplified 17q23 substantially decreases tumor growth in mouse xenografts. Collectively, our results reveal Trim37 as a new H2A ubiquitin ligase that is overexpressed in a subset of breast cancers and redirects PRC2 to silence tumor suppressors and other genes resulting in oncogenesis. Identification of TRIM37 Binding targets in MCF7 cells from the two replicate experiments

2014-10-06 | E-GEOD-48196 | biostudies-arrayexpress

A TRIM37 risk variant rs57141087 contributes to triple-negative breast cancer onset and progression in Black women.

Project description:TRIM37 is a histone H2A ubiquitin ligase importantin breast cancer oncogenesis. To assess the neoplastic transformationsof normal breast epithelial cells in the context of TRIM37, we increased its expression and compared the gene expression network regulated by TRIM37 in control and TRIM37 overexpression.

2025-01-15 | GSE277029 | GEO

TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene

2014-10-06 | GSE48196 | GEO

The ubiquitin ligase TRIM37 controls cancer-specific vulnerability to PLK4 inhibition

Project description:We show synthetic lethality between PLK4 inhibition-mediated centrosome loss and the overexpression of the ubiquitin ligase TRIM37 in cancer cells with amplification of Chr17q

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The ubiquitin ligase TRIM37 controls cancer-specific vulnerability to PLK4 inhibition

Project description:The ubiquitin ligase TRIM37 controls cancer-specific vulnerability to PLK4 inhibition

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TRIM28 orchestrates SUMO-ubiquitin crosstalk to stabilize PPARG and drive bladder cancer progression

Project description:Bladder cancer (BLCA) is a growing health burden with rising incidence and limited therapeutic options. To define the role of the Tripartite Motif (TRIM) family in BLCA, we integrated multi-cohort transcriptomic analyses with functional and mechanistic validation. TRIM28 was identified as the most consistently upregulated TRIM member in BLCA and correlated with poor prognosis. TRIM28 depletion suppressed, whereas its overexpression enhanced, BLCA cell proliferation. Mechanistically, TRIM28 directly bound to PPARG and acted as a SUMO E3 ligase to catalyze SUMOylation of PPARG at Lys94 within a noncanonical YKYD motif. This modification impaired PPARG recognition by the E3 ubiquitin ligase STUB1, reduced ubiquitin–proteasome degradation, and stabilized PPARG protein. Stabilized PPARG transcriptionally activated cholesterol biosynthetic genes, including DHCR7 and DHCR24, reprogramming cholesterol metabolism to promote BLCA progression. In summary, we identify a TRIM28-PPARG SUMO-ubiquitin crosstalk axis that drives metabolic remodeling and tumor growth in BLCA, highlighting TRIM28-mediated PPARG SUMOylation as a potential therapeutic target for metabolic intervention.

2026-02-11 | GSE318442 | GEO

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Project description:TRIM37 is a novel H2A ubiquitin ligase and a Breast Cancer Oncogene

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Induction of the mouse germ cell fate by transcription factors in vitro [exp2]

Project description:The germ cell lineage ensures the continuity of life through the generation of male and female gametes, which unite to form a totipotent zygote. We have established a culture system that recapitulates the mouse germ-cell specification pathway: Using cytokines, embryonic stem cells (ESCs)/induced pluripotent stem cells (iPSCs) are induced into epiblast-like cells (EpiLCs) and then into primordial germ cell-like cells (PGCLCs) with capacity both for spermatogenesis and oogenesis, creating an opportunity for understanding and regulating mammalian germ cell development in both sexes in vitro. Here we show that, without cytokines, simultaneous over-expression of three transcription factors (TFs), Blimp1 (also known as Prdm1), Prdm14 and Tfap2c (also known as AP2γ), directs EpiLCs, but not ESCs, swiftly and highly efficiently into a PGC state with endogenous transcription circuitry. The induction of the PGC state on EpiLCs minimally requires Prdm14 but not Blimp1 or Tfap2c. The TF-induced PGC state reconstitutes key transcriptome and epigenetic reprogramming in PGCs, but bypasses a mesodermal program that accompanies PGC specification in vivo and in vitro by cytokines including BMP4. Importantly, the TF-induced PGC-like cells robustly contribute to spermatogenesis and fertile offspring. Our findings provide not only a novel insight into the transcriptional logic that creates a germ cell state, but also a foundation for the TF-based reconstitution and regulation of mammalian gametogenesis.

2013-08-04 | GSE46854 | GEO

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