The primordial growth disorder 3-M syndrome connects ubiquitination to the cytoskeletal adaptor OBSL1

  • Am J Hum Genet. 2009 Jun;84(6):801-6. doi: 10.1016/j.ajhg.2009.04.021.
Dan Hanson  1 ,  Philip G Murray ,  Amit Sud ,  Samia A Temtamy ,  Mona Aglan ,  Andrea Superti-Furga ,  Sue E Holder ,  Jill Urquhart ,  Emma Hilton ,  Forbes D C Manson ,  Peter Scambler ,  Graeme C M Black ,  Peter E Clayton
Affiliations
  • 1. Endocrine Sciences, Faculty of Medical & Human Sciences, University of Manchester, Manchester, UK.
Abstract

3-M syndrome is an autosomal-recessive primordial growth disorder characterized by significant intrauterine and postnatal growth restriction. Mutations in the CUL7 gene are known to cause 3-M syndrome. In 3-M syndrome patients that do not carry CUL7 mutations, we performed high-density genome-wide SNP mapping to identify a second locus at 2q35-q36.1. Further haplotype analysis revealed a 1.29 Mb interval in which the underlying gene is located and we subsequently discovered seven distinct null mutations from 10 families within the gene OBSL1. OBSL1 is a putative cytoskeletal adaptor protein that localizes to the nuclear envelope. We were also able to demonstrate that loss of OBSL1 leads to downregulation of CUL7, implying a role for OBSL1 in the maintenance of CUL7 protein levels and suggesting that both proteins are involved within the same molecular pathway.