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sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress

Although some RNA-binding proteins are known to contribute to neurodegeneration, the genetic interaction between the genes encoding these proteins is unclear. Here, we examine the interaction between sym-2, the gene encoding an ortholog of hnRNPF and hnRNPH, and hrpa-1, the ortholog of of the gene e...

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Detalles Bibliográficos
Autores principales: Ryan, Veronica H., Hart, Anne C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Caltech Library 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7859837/
https://www.ncbi.nlm.nih.gov/pubmed/33554054
http://dx.doi.org/10.17912/micropub.biology.000363
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author Ryan, Veronica H.
Hart, Anne C.
author_facet Ryan, Veronica H.
Hart, Anne C.
author_sort Ryan, Veronica H.
collection PubMed
description Although some RNA-binding proteins are known to contribute to neurodegeneration, the genetic interaction between the genes encoding these proteins is unclear. Here, we examine the interaction between sym-2, the gene encoding an ortholog of hnRNPF and hnRNPH, and hrpa-1, the ortholog of of the gene encoding hnRNPA2, which when mutated causes multisystem proteinopathy. We find that after 22 hours, but not 4 hours, of paraquat-induced oxidative stress, sym-2(mn617) has a mild glutamatergic neurodegeneration phenotype. Interestingly, this defect is rescued by expression of chimeric WT hrpa-1, but not mutant. Thus, we identify a curious genetic interaction between sym-2 and hrpa-1.
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spelling pubmed-78598372021-02-05 sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress Ryan, Veronica H. Hart, Anne C. MicroPubl Biol New Finding Although some RNA-binding proteins are known to contribute to neurodegeneration, the genetic interaction between the genes encoding these proteins is unclear. Here, we examine the interaction between sym-2, the gene encoding an ortholog of hnRNPF and hnRNPH, and hrpa-1, the ortholog of of the gene encoding hnRNPA2, which when mutated causes multisystem proteinopathy. We find that after 22 hours, but not 4 hours, of paraquat-induced oxidative stress, sym-2(mn617) has a mild glutamatergic neurodegeneration phenotype. Interestingly, this defect is rescued by expression of chimeric WT hrpa-1, but not mutant. Thus, we identify a curious genetic interaction between sym-2 and hrpa-1. Caltech Library 2021-02-03 /pmc/articles/PMC7859837/ /pubmed/33554054 http://dx.doi.org/10.17912/micropub.biology.000363 Text en Copyright: © 2021 by the authors https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle New Finding
Ryan, Veronica H.
Hart, Anne C.
sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
title sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
title_full sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
title_fullStr sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
title_full_unstemmed sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
title_short sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
title_sort sym-2 loss-of-function causes glutamatergic neurodegeneration after oxidative stress
topic New Finding
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7859837/
https://www.ncbi.nlm.nih.gov/pubmed/33554054
http://dx.doi.org/10.17912/micropub.biology.000363
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