A new mouse mutant with a discrete mutation in Pcdhgc5 reveals that the Protocadherin γC5 isoform is not essential for dendrite arborization in the cerebral cortex

Camille M Hanes; David M Steffen; George C Murray; Robert W Burgess; Joshua A Weiner; Andrew M Garrett

doi:10.1371/journal.pone.0344863

Back

A new mouse mutant with a discrete mutation in Pcdhgc5 reveals that the Protocadherin γC5 isoform is not essential for dendrite arborization in the cerebral cortex

Journal article

Open access

Peer reviewed

A new mouse mutant with a discrete mutation in Pcdhgc5 reveals that the Protocadherin γC5 isoform is not essential for dendrite arborization in the cerebral cortex

Camille M Hanes, David M Steffen, George C Murray, Robert W Burgess, Joshua A Weiner and Andrew M Garrett

PloS one, Vol.21(3), e0344863

03/12/2026

DOI: 10.1371/journal.pone.0344863

PMCID: PMC12981507

PMID: 41818197

Files and links (1)

url

https://doi.org/10.1371/journal.pone.0344863View

Published (Version of record) Open Access

Abstract

There are ~ 60 clustered protocadherin (cPcdh) isoforms expressed from three gene clusters (Pcdha, Pcdhb, Pcdhg) arrayed in tandem across nearly 1 Mb in mammals. cPcdhs are homophilic cell adhesion molecules (CAMs) critical for a host of neural developmental functions consistent with a role in cell-cell recognition. Indeed, isoforms make recognition modules in combination to generate recognition diversity far exceeding the ~ 60 individual CAMs. However, there is also growing evidence for specialized functions for specific isoforms, particularly the C-type isoforms found at the 3' ends of the Pcdha cluster (αC1 and αC2) and at the 3' end of the Pcdhg cluster (γC3, γC4, and γC5). We have previously described unique roles for γC3 in dendrite arborization in the cerebral cortex and neural circuit formation in the spinal cord, as well as for γC4 in neuronal survival. Here we report a new mouse mutant specifically targeting the Pcdhgc5 exon encoding γC5. Unlike the rest of the Pcdhg cluster, expression of this isoform does not begin until postnatal stages of mouse development, increasing in the second week of life, suggesting specialized roles. We found significant expression changes in gene pathways involved in synaptic activity, learning and memory, and cognition. Despite this, we saw no major disruption in the cerebral cortex in neuronal organization, survival, dendritic arborization, or synaptic protein expression in these mutants. This new model will be an important tool for future studies delineating specific functions for γC5.

Mutation

Animals

Cadherin Related Proteins

Cadherins - genetics

Cadherins - metabolism

Cerebral Cortex - cytology

Cerebral Cortex - growth & development

Cerebral Cortex - metabolism

Dendrites - metabolism

Mice

Protein Isoforms - genetics

Protein Isoforms - metabolism

Details

Title: Subtitle: A new mouse mutant with a discrete mutation in Pcdhgc5 reveals that the Protocadherin γC5 isoform is not essential for dendrite arborization in the cerebral cortex
Creators: Camille M Hanes - University of Iowa
David M Steffen - University of Iowa
George C Murray - Jackson Laboratory
Robert W Burgess - Jackson Laboratory
Joshua A Weiner - University of Iowa
Andrew M Garrett - Wayne State University
Resource Type: Journal article
Publication Details: PloS one, Vol.21(3), e0344863
DOI: 10.1371/journal.pone.0344863
PMID: 41818197
PMCID: PMC12981507
NLM abbreviation: PLoS One
ISSN: 1932-6203
eISSN: 1932-6203
Publisher: Public Library of Science
Language: English
Date published: 03/12/2026
Academic Unit: Liberal Arts and Science Admin; Psychiatry; Iowa Neuroscience Institute; Biology
Record Identifier: 9985147185202771

Metrics

1 Record Views