Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in
During nervous system development, axons must navigate to specific target areas. In Caenorhabditis elegans , the cadherin CDH-4 is required for ventral nerve cord axonal navigation, and dorsal nerve cord fasciculation. How CDH-4 mediates axon navigation and fasciculation is currently unknown. To ide...
Main Authors: | , , |
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Format: | Article |
Language: | English |
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SAGE Publishing
2022-09-01
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Series: | Neuroscience Insights |
Online Access: | https://doi.org/10.1177/26331055221123346 |
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author | Zina Aburegeba Jie Pan Harald Hutter |
author_facet | Zina Aburegeba Jie Pan Harald Hutter |
author_sort | Zina Aburegeba |
collection | DOAJ |
description | During nervous system development, axons must navigate to specific target areas. In Caenorhabditis elegans , the cadherin CDH-4 is required for ventral nerve cord axonal navigation, and dorsal nerve cord fasciculation. How CDH-4 mediates axon navigation and fasciculation is currently unknown. To identify genes acting together with cdh-4 , we isolated mutants suppressing the axon guidance defects of cdh-4 mutants. These suppressors showed partial suppression of axonal defects in the dorsal and ventral nerve cords seen in cdh-4 mutants. We identified one suppressor gene, prp-6 , which encodes a component of the spliceosome. Complete loss-of-function alleles of prp-6 are lethal, suggesting that the mutation isolated in our suppressor screen is a partial loss-of-function allele. A previous study found that RNAi-induced suppression of prp-6 leads to changes in the expression of several 100 genes including the cadherin cdh-5 . We found that overexpression of cdh-5 mimics the suppression seen in prp-6 mutants, suggesting that CDH-5 can partially compensate for the loss of CDH-4. |
first_indexed | 2024-04-11T21:27:55Z |
format | Article |
id | doaj.art-b85c7a8e10ba4e86a80fc9c08b5aaf7d |
institution | Directory Open Access Journal |
issn | 2633-1055 |
language | English |
last_indexed | 2024-04-11T21:27:55Z |
publishDate | 2022-09-01 |
publisher | SAGE Publishing |
record_format | Article |
series | Neuroscience Insights |
spelling | doaj.art-b85c7a8e10ba4e86a80fc9c08b5aaf7d2022-12-22T04:02:20ZengSAGE PublishingNeuroscience Insights2633-10552022-09-011710.1177/26331055221123346Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in Zina Aburegeba0Jie Pan1Harald Hutter2Department of Biological Sciences, Simon Fraser University, Burnaby, BC, CanadaDepartment of Biological Sciences, Simon Fraser University, Burnaby, BC, CanadaDepartment of Biological Sciences, Simon Fraser University, Burnaby, BC, CanadaDuring nervous system development, axons must navigate to specific target areas. In Caenorhabditis elegans , the cadherin CDH-4 is required for ventral nerve cord axonal navigation, and dorsal nerve cord fasciculation. How CDH-4 mediates axon navigation and fasciculation is currently unknown. To identify genes acting together with cdh-4 , we isolated mutants suppressing the axon guidance defects of cdh-4 mutants. These suppressors showed partial suppression of axonal defects in the dorsal and ventral nerve cords seen in cdh-4 mutants. We identified one suppressor gene, prp-6 , which encodes a component of the spliceosome. Complete loss-of-function alleles of prp-6 are lethal, suggesting that the mutation isolated in our suppressor screen is a partial loss-of-function allele. A previous study found that RNAi-induced suppression of prp-6 leads to changes in the expression of several 100 genes including the cadherin cdh-5 . We found that overexpression of cdh-5 mimics the suppression seen in prp-6 mutants, suggesting that CDH-5 can partially compensate for the loss of CDH-4.https://doi.org/10.1177/26331055221123346 |
spellingShingle | Zina Aburegeba Jie Pan Harald Hutter Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in Neuroscience Insights |
title | Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in |
title_full | Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in |
title_fullStr | Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in |
title_full_unstemmed | Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in |
title_short | Mutations in the Spliceosome Component and Overexpression of Suppress Axon Guidance Defects of Mutants in |
title_sort | mutations in the spliceosome component and overexpression of suppress axon guidance defects of mutants in |
url | https://doi.org/10.1177/26331055221123346 |
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