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Heterozygote Wdr36-deficient mice do not develop glaucoma.
- Source :
-
Experimental Eye Research . Nov2014, Vol. 128, p83-91. 9p. - Publication Year :
- 2014
-
Abstract
- There is an ongoing controversy regarding the role of WDR36 sequence variants in the pathogenesis of primary open-angle glaucoma (POAG). WDR36 is a nucleolar protein involved in the maturation of 18S rRNA. The function of WDR36 is essential as homozygous Wdr36 -deficient mouse embryos die before reaching the blastocyst stage. Here we provide a detailed analysis of the phenotype of heterozygous Wdr36 -deficient mice. Loss of one Wdr36 allele causes a substantial reduction in the expression of Wdr36 mRNA. In the eyes of Wdr36 +/− animals, the structure of the tissues involved in aqueous humor circulation and of the optic nerve head are not different from that of control littermates. In addition, one-year-old Wdr36 +/− animals do not differ from wild-type animals with regards to intraocular pressure and number of optic nerve axons. The susceptibility of retinal ganglion cells to excitotoxic damage induced by NMDA is similar in Wdr36 +/− and wild-type animals. Moreover, the amount of optic nerve axonal damage induced by high IOP is not different between Wdr36 +/− and wild-type mice. Transgenic overexpression of mutated Del605-607 Wdr36 in Wdr36 +/− animals does not cause changes in the number of optic nerve axons or susceptibility to excitotoxic damage. In addition, analysis of 18S rRNA maturation in Del605-607 Wdr36 +/− or Wdr36 +/− mice does not show obvious differences in rRNA processing or in the amounts of precursor forms when compared to wild-type animals. Our data obtained in Wdr36 +/− mice do not support the assumption of a causative role for WDR36 in the pathogenesis of POAG. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00144835
- Volume :
- 128
- Database :
- Academic Search Index
- Journal :
- Experimental Eye Research
- Publication Type :
- Academic Journal
- Accession number :
- 99100684
- Full Text :
- https://doi.org/10.1016/j.exer.2014.09.008