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Nature genetics · 2010

Mutations in TMEM216 perturb ciliogenesis and cause Joubert, Meckel and related syndromes.

СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Valente Enza Maria, Logan Clare V, Mougou-Zerelli Soumaya, Lee Jeong Ho, Silhavy Jennifer L, Brancati Francesco, Iannicelli Miriam, Travaglini Lorena, Romani Sveva, Illi Barbara, Adams Matthew, Szymanska Katarzyna, Mazzotta Annalisa, Lee Ji Eun, Tolentino Jerlyn C, Swistun Dominika, Salpietro Carmelo D, Fede Carmelo, Gabriel Stacey, Russ Carsten, Cibulskis Kristian, Sougnez Carrie, Hildebrandt Friedhelm, Otto Edgar A, Held Susanne, Diplas Bill H, Davis Erica E, Mikula Mario, Strom Charles M, Ben-Zeev Bruria, Lev Dorit, Sagie Tally Lerman, Michelson Marina, Yaron Yuval, Krause Amanda, Boltshauser Eugen, Elkhartoufi Nadia, Roume Joelle, Shalev Stavit, Munnich Arnold, Saunier Sophie, Inglehearn Chris, Saad Ali, Alkindy Adila, Thomas Sophie, Vekemans Michel, Dallapiccola Bruno, Katsanis Nicholas, Johnson Colin A, Attié-Bitach Tania, Gleeson Joseph G

Аннотация

Joubert syndrome (JBTS), related disorders (JSRDs) and Meckel syndrome (MKS) are ciliopathies. We now report that MKS2 and CORS2 (JBTS2) loci are allelic and caused by mutations in TMEM216, which encodes an uncharacterized tetraspan transmembrane protein. Individuals with CORS2 frequently had nephronophthisis and polydactyly, and two affected individuals conformed to the oro-facio-digital type VI phenotype, whereas skeletal dysplasia was common in fetuses affected by MKS. A single G218T mutation (R73L in the protein) was identified in all cases of Ashkenazi Jewish descent (n=10). TMEM216 localized to the base of primary cilia, and loss of TMEM216 in mutant fibroblasts or after knockdown caused defective ciliogenesis and centrosomal docking, with concomitant hyperactivation of RhoA and Dishevelled. TMEM216 formed a complex with Meckelin, which is encoded by a gene also mutated in JSRDs and MKS. Disruption of tmem216 expression in zebrafish caused gastrulation defects similar to those in other ciliary morphants. These data implicate a new family of proteins in the ciliopathies and further support allelism between ciliopathy disorders.

Предметные рубрики MeSH

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты