<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhou Z</submitter><funding>SUMC Start-up Funding</funding><funding>MOST | National Key Research and Development Program of China (NKPs)</funding><funding>MOST | National Key Research and Development Program of China</funding><funding>MOST | National Natural Science Foundation of China (NSFC)</funding><funding>MOST | National Natural Science Foundation of China</funding><pagination>2861-2877</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11239855</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(7)</volume><pubmed_abstract>In developing olfactory bulb (OB), mitral cells (MCs) remodel their dendrites to establish the precise olfactory circuit, and these circuits are critical for individuals to sense odors and elicit behaviors for survival. However, how microtubules (MTs) participate in the process of dendritic remodeling remains elusive. Here, we reveal that calmodulin-regulated spectrin-associated proteins (CAMSAPs), a family of proteins that bind to the minus-end of the noncentrosomal MTs, play a crucial part in the development of MC dendrites. We observed that Camsap2 knockout (KO) males are infertile while the reproductive tract is normal. Further study showed that the infertility was due to the severe defects of mating behavior in male mice. Besides, mice with loss-of-function displayed defects in the se</pubmed_abstract><journal>EMBO reports</journal><pubmed_title>Deficiency of CAMSAP2 impairs olfaction and the morphogenesis of mitral cells.</pubmed_title><pmcid>PMC11239855</pmcid><funding_grant_id>510858072</funding_grant_id><funding_grant_id>32100760</funding_grant_id><funding_grant_id>2018YFA0801104</funding_grant_id><funding_grant_id>2021YFA0804802</funding_grant_id><funding_grant_id>32270736</funding_grant_id><funding_grant_id>31930025</funding_grant_id><pubmed_authors>Lin R</pubmed_authors><pubmed_authors>Shao J</pubmed_authors><pubmed_authors>Xu P</pubmed_authors><pubmed_authors>Hu W</pubmed_authors><pubmed_authors>Yang M</pubmed_authors><pubmed_authors>Xu H</pubmed_authors><pubmed_authors>Xie Q</pubmed_authors><pubmed_authors>Zhang R</pubmed_authors><pubmed_authors>Zhou Z</pubmed_authors><pubmed_authors>Meng W</pubmed_authors><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Lin C</pubmed_authors><pubmed_authors>Mao A</pubmed_authors><pubmed_authors>Xu Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Deficiency of CAMSAP2 impairs olfaction and the morphogenesis of mitral cells.</name><description>In developing olfactory bulb (OB), mitral cells (MCs) remodel their dendrites to establish the precise olfactory circuit, and these circuits are critical for individuals to sense odors and elicit behaviors for survival. However, how microtubules (MTs) participate in the process of dendritic remodeling remains elusive. Here, we reveal that calmodulin-regulated spectrin-associated proteins (CAMSAPs), a family of proteins that bind to the minus-end of the noncentrosomal MTs, play a crucial part in the development of MC dendrites. We observed that Camsap2 knockout (KO) males are infertile while the reproductive tract is normal. Further study showed that the infertility was due to the severe defects of mating behavior in male mice. Besides, mice with loss-of-function displayed defects in the se</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-06-02T22:04:43.82Z</modification><creation>2026-05-28T03:06:24.518Z</creation></dates><accession>S-EPMC11239855</accession><cross_references><pubmed>38839944</pubmed><doi>10.1038/s44319-024-00166-x</doi></cross_references></HashMap>