Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Gene: Rpl24 - ribosomal protein L24

Mus musculus

Synonyms: 0610008L05Rik, 60S ribosomal protein L24, Bst

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Rice, D.S., Aijaz, S., Delettre, C., Oliver, E.R., Smith, R.S., et al.

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Disease relevance of Rpl24

Delayed fusion of the fissure is consistently associated with the Bst/+ genotype and probably contributes to the failure of ganglion cell axons to grow out of the eye [1].
Mapping the Bst mutation on mouse chromosome 16: a model for human optic atrophy [2].

High impact information on Rpl24

We report an angiogenic phenotype in Bst/+ mice that is age-related, clinically evident, and resembles human SRN [3].
Bst significantly impairs Rpl24 splicing and ribosome biogenesis [4].
Ribosomal protein L24 defect in belly spot and tail (Bst), a mouse Minute [4].
The reduction in ganglion cell number in affected adult Bst/+ mice is attributable to the failure of ganglion cell axons to reach the optic nerve head early in development [1].
Decreased retinal ganglion cell number and misdirected axon growth associated with fissure defects in Bst/+ mutant mice [1].

Biological context of Rpl24

Screening of the whole mRNA coding sequence and of the 31 exons of Opa1 did not reveal any mutation in Bst [5].

Anatomical context of Rpl24

The autosomal semidominant mutation Bst (belly spot and tail) is often associated with small and atrophic optic nerves in adult mice and shares several important attributes with heritable optic nerve atrophy in humans [1].
Retinal ganglion cells in adult Bst/+ mice were labeled retrogradely with horseradish peroxidase injected into the right optic tract [1].

Other interactions of Rpl24

Gene structure and chromosomal localization of mouse Opa1 : its exclusion from the Bst locus [5].

Analytical, diagnostic and therapeutic context of Rpl24

METHODS: A polyclonal antibody generated against a C-terminal peptide of OPA1 was used to assess by immunohistochemistry the expression of mOPA1 in the wild-type embryonic and postnatal mouse ocular tissues and the Bst/+ retina [6].
Nested PCR products were differentiated by Hph I and Bst EII digestion [7].

References

Decreased retinal ganglion cell number and misdirected axon growth associated with fissure defects in Bst/+ mutant mice. Rice, D.S., Tang, Q., Williams, R.W., Harris, B.S., Davisson, M.T., Goldowitz, D. Invest. Ophthalmol. Vis. Sci. (1997)
Mapping the Bst mutation on mouse chromosome 16: a model for human optic atrophy. Rice, D.S., Williams, R.W., Ward-Bailey, P., Johnson, K.R., Harris, B.S., Davisson, M.T., Goldowitz, D. Mamm. Genome (1995)
The bst locus on mouse chromosome 16 is associated with age-related subretinal neovascularization. Smith, R.S., John, S.W., Zabeleta, A., Davisson, M.T., Hawes, N.L., Chang, B. Proc. Natl. Acad. Sci. U.S.A. (2000)
Ribosomal protein L24 defect in belly spot and tail (Bst), a mouse Minute. Oliver, E.R., Saunders, T.L., Tarlé, S.A., Glaser, T. Development (2004)
Gene structure and chromosomal localization of mouse Opa1 : its exclusion from the Bst locus. Delettre, C., Lenaers, G., Belenguer, P., Hamel, C.P. BMC Genet. (2003)
Developmental expression profile of the optic atrophy gene product: OPA1 is not localized exclusively in the mammalian retinal ganglion cell layer. Aijaz, S., Erskine, L., Jeffery, G., Bhattacharya, S.S., Votruba, M. Invest. Ophthalmol. Vis. Sci. (2004)
Detection and differentiation of Aino and Akabane Simbu serogroup bunyaviruses by nested polymerase chain reaction. Akashi, H., Onuma, S., Nagano, H., Ohta, M., Fukutomi, T. Arch. Virol. (1999)