Fam151b, the mouse homologue of C.elegans menorin gene, is essential for retinal function

Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal branching. The International Mouse Phenotyping Consortium (IMPC) aims to knock out every gene in the mouse and comprehensively phenotype the mutant animals. This project identified Fam151b homozygous knock...

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Published inScientific reports Vol. 10; no. 1; p. 437
Main Authors Findlay, Amy S., McKie, Lisa, Keighren, Margaret, Clementson-Mobbs, Sharon, Sanchez-Pulido, Luis, Wells, Sara, Cross, Sally H., Jackson, Ian J.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 16.01.2020
Nature Publishing Group
Subjects
45/70
631/208
64/60
692/699/3161
Amino Acid Sequence
Animals
Caenorhabditis elegans Proteins - genetics
Cell Count
Electroretinograms
Eye
Gene Knockout Techniques
Humanities and Social Sciences
Humans
Mammals
Membrane Proteins - genetics
Mice
Models, Molecular
multidisciplinary
Mutants
Mutation
Phenotypes
Phenotyping
Phosphodiesterase
Photoreceptor Cells, Vertebrate - cytology
Photoreceptors
Protein Conformation
Retina
Retina - cytology
Retina - physiology
Retinal degeneration
Science
Science (multidisciplinary)
Sequence analysis
Sequence Homology, Nucleic Acid
Online AccessGet full text

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Abstract Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal branching. The International Mouse Phenotyping Consortium (IMPC) aims to knock out every gene in the mouse and comprehensively phenotype the mutant animals. This project identified Fam151b homozygous knock-out mice as having retinal degeneration. We show they have no photoreceptor function from eye opening, as demonstrated by a lack of electroretinograph (ERG) response. Histological analysis shows that during development of the eye the correct number of cells are produced and that the layers of the retina differentiate normally. However, after eye opening at P14, Fam151b mutant eyes exhibit signs of retinal stress and rapidly lose photoreceptor cells. We have mutated the second mammalian menorin homologue, Fam151a , and homozygous mutant mice have no discernible phenotype. Sequence analysis indicates that the FAM151 proteins are members of the PLC-like phosphodiesterase superfamily. However, the substrates and function of the proteins remains unknown.
AbstractList Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal branching. The International Mouse Phenotyping Consortium (IMPC) aims to knock out every gene in the mouse and comprehensively phenotype the mutant animals. This project identified Fam151b homozygous knock-out mice as having retinal degeneration. We show they have no photoreceptor function from eye opening, as demonstrated by a lack of electroretinograph (ERG) response. Histological analysis shows that during development of the eye the correct number of cells are produced and that the layers of the retina differentiate normally. However, after eye opening at P14, Fam151b mutant eyes exhibit signs of retinal stress and rapidly lose photoreceptor cells. We have mutated the second mammalian menorin homologue, Fam151a , and homozygous mutant mice have no discernible phenotype. Sequence analysis indicates that the FAM151 proteins are members of the PLC-like phosphodiesterase superfamily. However, the substrates and function of the proteins remains unknown.
Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal branching. The International Mouse Phenotyping Consortium (IMPC) aims to knock out every gene in the mouse and comprehensively phenotype the mutant animals. This project identified Fam151b homozygous knock-out mice as having retinal degeneration. We show they have no photoreceptor function from eye opening, as demonstrated by a lack of electroretinograph (ERG) response. Histological analysis shows that during development of the eye the correct number of cells are produced and that the layers of the retina differentiate normally. However, after eye opening at P14, Fam151b mutant eyes exhibit signs of retinal stress and rapidly lose photoreceptor cells. We have mutated the second mammalian menorin homologue, Fam151a, and homozygous mutant mice have no discernible phenotype. Sequence analysis indicates that the FAM151 proteins are members of the PLC-like phosphodiesterase superfamily. However, the substrates and function of the proteins remains unknown.
ArticleNumber 437
Author Findlay, Amy S.
Jackson, Ian J.
Clementson-Mobbs, Sharon
Cross, Sally H.
Sanchez-Pulido, Luis
Keighren, Margaret
McKie, Lisa
Wells, Sara
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CitedBy_id crossref_primary_10_1371_journal_pone_0268149
crossref_primary_10_1016_j_smallrumres_2024_107257
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Snippet Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal branching. The International Mouse Phenotyping Consortium (IMPC)...
Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal branching. The International Mouse Phenotyping Consortium (IMPC)...
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StartPage 437
SubjectTerms 45/70
631/208
64/60
692/699/3161
Amino Acid Sequence
Animals
Caenorhabditis elegans Proteins - genetics
Cell Count
Electroretinograms
Eye
Gene Knockout Techniques
Humanities and Social Sciences
Humans
Mammals
Membrane Proteins - genetics
Mice
Models, Molecular
multidisciplinary
Mutants
Mutation
Phenotypes
Phenotyping
Phosphodiesterase
Photoreceptor Cells, Vertebrate - cytology
Photoreceptors
Protein Conformation
Retina
Retina - cytology
Retina - physiology
Retinal degeneration
Science
Science (multidisciplinary)
Sequence analysis
Sequence Homology, Nucleic Acid
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Title Fam151b, the mouse homologue of C.elegans menorin gene, is essential for retinal function
URI https://link.springer.com/article/10.1038/s41598-019-57398-4
https://www.ncbi.nlm.nih.gov/pubmed/31949211
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https://search.proquest.com/docview/2341618298
https://pubmed.ncbi.nlm.nih.gov/PMC6965129
Volume 10
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