Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Ctnnb1-targeted genes in mouse post-meiotic germ cells

ABSTRACT: To determine differential gene expression in Ctnnb1 CKO mice testis compared to CTRL mice testis. The Agilent Mouse Whole Genome 4x44K array (Samples are from pooled total testes RNA from 4 CTRL and 4 Ctnnb1 CKO mice; dye-swap was performed.)

ORGANISM(S): Mus musculus

SUBMITTER: Hung-I Chen

PROVIDER: E-GEOD-30773 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Role of β-catenin in post-meiotic male germ cell differentiation.

Chang Yao-Fu YF Lee-Chang Jennifer S JS Harris Krystle Y KY Sinha-Hikim Amiya P AP Rao Manjeet K MK

PloS one 20111118 11

Though roles of β-catenin signaling during testis development have been well established, relatively little is known about its role in postnatal testicular physiology. Even less is known about its role in post-meiotic germ cell development and differentiation. Here, we report that β-catenin is highly expressed in post-meiotic germ cells and plays an important role during spermiogenesis in mice. Spermatid-specific deletion of β-catenin resulted in significantly reduced sperm count, increased germ ...[more]

PMID: 22125654

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Project description:Stable activation of the WNT signaling effector beta-catenin (CTNNB1(ex3) in ovarian granulosa cells results in the formation of premalignant lesions that develop into granulosa cell tumors (GCTs) spontaneously later in life. Loss of the tumor suppressor gene Pten accelerates GCT formation in the CTNNB1 strain. Conversely, expression of oncogenic KRASG12D causes the dramatic arrest of proliferation, differentiation and apoptosis in granulosa cells, and consequently, small abnormal follicle-like structures devoid of oocytes accumulate in the ovary. Because of the potent anti-proliferative effects of KRASG12D in granulosa cells, we sought to determine if KRASG12D would block precancerous lesion and tumor formation in follicles of the CTNNB1 mutant mice. Unexpectedly, transgenic Ctnnb1;Kras mutant mice developed early-onset GCTs leading to premature death in a manner similar to theCtnnb1;Pten mutant mice. Moreover, the GCTs in the Ctnnb1;Kras mutant mice exhibited increased GC proliferation, decreased apoptosis and impaired differentiation. Microarray and RT-PCR analyses revealed that ovaries from mice expressing dominant-stable CTNNB1 with either Pten loss or KRAS activation were unpredictably similar. Specifically, gene regulatory processes induced by CTNNB1 were mostly enhanced by either KRAS activation or Pten loss in remarkably similar patterns and degree. Furthermore, the concomitant activation of CTNNB1 and KRAS in Sertoli cells resulted in the development of granulosa cell tumors of the testis. RT-PCR studies showed a partial overlap in gene regulatory processes associated with tumor development in the ovary and testis. Together, these results suggest that KRAS activation and Pten loss induce GCT development from premalignant lesions via highly similar molecular mechanisms. four samples: average of two wild type samples (previously submitted as GSM403220 and GSM403221), beta-Catenin constitutively active mutant, beta-Catenin;Pten double mutant, and beta-Catenin;Kras(G12D) double mutant

Dataset Information

Ctnnb1-targeted genes in mouse post-meiotic germ cells

Publications

Role of β-catenin in post-meiotic male germ cell differentiation.

Similar Datasets

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