Publication:
PPP2R3C gene variants cause syndromic 46,XY gonadal dysgenesis and impaired spermatogenesis in humans

dc.contributor.authorsGuran, Tulay; Yesil, Gozde; Turan, Serap; Atay, Zeynep; Bozkurtlar, Emine; Aghayev, AghaRza; Gul, Sinem; Tinay, Ilker; Aru, Basak; Arslan, Sema; Koroglu, M. Kutay; Ercan, Feriha; Demirel, Gulderen Y.; Eren, Funda S.; Karademir, Betul; Bereket, Abdullah
dc.date.accessioned2022-03-14T10:20:07Z
dc.date.accessioned2026-01-11T19:15:42Z
dc.date.available2022-03-14T10:20:07Z
dc.date.issued2019-05
dc.description.abstractContext: Most of the knowledge on the factors involved in human sexual development stems from studies of rare cases with disorders of sex development. Here, we have described a novel 46, XY complete gonadal dysgenesis syndrome caused by homozygous variants in PPP2R3C gene. This gene encodes B '' gamma regulatory subunit of the protein phosphatase 2A (PP2A), which is a serine/threonine phosphatase involved in the phospho-regulation processes of most mammalian cell types. PPP2R3C gene is most abundantly expressed in testis in humans, while its function was hitherto unknown. Patients and methods: Four girls from four unrelated families with 46, XY complete gonadal dysgenesis were studied using exome or Sanger sequencing of PPP2R3C gene. In total, four patients and their heterozygous parents were investigated for clinical, laboratory, immunohistochemical and molecular characteristics. Results: We have identified three different homozygous PPP2R3C variants, c.308T>C (p.L103P), c.578T>C (p.L193S) and c.1049T>C (p.F350S), in four girls with 46, XY complete gonadal dysgenesis. Patients also manifested a unique syndrome of extragonadal anomalies, including typical facial gestalt, low birth weight, myopathy, rod and cone dystrophy, anal atresia, omphalocele, sensorineural hearing loss, dry and scaly skin, skeletal abnormalities, renal agenesis and neuromotor delay. We have shown a decreased SOX9-Phospho protein expression in the dysgenetic gonads of the patients with homozygous PPP2R3C variants suggesting impaired SOX9 signaling in the pathogenesis of gonadal dysgenesis. Heterozygous males presented with abnormal sperm morphology and impaired fertility. Conclusion: Our findings suggest that PPP2R3C protein is involved in the ontogeny of multiple organs, especially critical for testis development and spermatogenesis. PPPR3C provides insight into pathophysiology, as well as emerging as a potential therapeutic target for male infertility.
dc.identifier.doi10.1530/EJE-19-0067
dc.identifier.eissn1479-683X
dc.identifier.issn0804-4643
dc.identifier.pubmed30893644
dc.identifier.urihttps://hdl.handle.net/11424/244357
dc.identifier.wosWOS:000464997600005
dc.language.isoeng
dc.publisherBIOSCIENTIFICA LTD
dc.relation.ispartofEUROPEAN JOURNAL OF ENDOCRINOLOGY
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectPROTEIN PHOSPHATASE 2A
dc.subjectMICROTUBULE-ASSOCIATED PROTEIN
dc.subjectSUBUNIT
dc.subjectPHOSPHORYLATION
dc.subjectTAU
dc.subjectEXPRESSION
dc.subjectDISORDERS
dc.subjectSOX9
dc.subjectG5PR
dc.titlePPP2R3C gene variants cause syndromic 46,XY gonadal dysgenesis and impaired spermatogenesis in humans
dc.typearticle
dspace.entity.typePublication
oaire.citation.endPage309
oaire.citation.issue5
oaire.citation.startPage291
oaire.citation.titleEUROPEAN JOURNAL OF ENDOCRINOLOGY
oaire.citation.volume180

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