| Literature DB >> 28275241 |
Kandai Nozu1, Shogo Minamikawa1, Shiro Yamada2,3, Masafumi Oka1, Motoko Yanagita4, Naoya Morisada1, Shuichiro Fujinaga5, China Nagano6, Yoshimitsu Gotoh6, Eihiko Takahashi7, Takahiro Morishita8, Tomohiko Yamamura1, Takeshi Ninchoji1, Hiroshi Kaito1, Ichiro Morioka1, Koichi Nakanishi9, Igor Vorechovsky10, Kazumoto Iijima1.
Abstract
Alport syndrome-diffuse leiomyomatosis (AS-DL, OMIM: 308940) is a rare variant of the X-linked Alport syndrome that shows overgrowth of visceral smooth muscles in the gastrointestinal, respiratory and female reproductive tracts in addition to renal symptoms. AS-DL results from deletions that encompass the 5' ends of the COL4A5 and COL4A6 genes, but deletion breakpoints between COL4A5 and COL4A6 have been determined in only four cases. Here, we characterize deletion breakpoints in five AS-DL patients and show a contiguous COL4A6/COL4A5 deletion in each case. We also demonstrate that eight out of nine deletion alleles involved sequences homologous between COL4A5 and COL4A6. Most breakpoints took place in recognizable transposed elements, including long and short interspersed repeats, DNA transposons and long-terminal repeat retrotransposons. Because deletions involved the bidirectional promoter region in each case, we suggest that the occurrence of leiomyomatosis in AS-DL requires inactivation of both genes. Altogether, our study highlights the importance of homologous recombination involving multiple transposed elements for the development of this continuous gene syndrome and other atypical loss-of-function phenotypes.Entities:
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Year: 2017 PMID: 28275241 DOI: 10.1038/jhg.2017.28
Source DB: PubMed Journal: J Hum Genet ISSN: 1434-5161 Impact factor: 3.172