Targeted Deletion in the Basal Body Protein Talpid3 Leads to Loss of Primary Cilia in Embryonic Stem Cells and Defective Lineage-Specific Differentiation
Talpid3 is a basal body protein required for the formation of primary cilia, an organelle involved in signal transduction. Here, we asked if Talpid3 has a role in the regulation of differentiation and/or self-renewal of ES cells and whether cells lacking cilia due to a deletion in Talpid3 can be rep...
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2024-11-01
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| Series: | Cells |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2073-4409/13/23/1957 |
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| Summary: | Talpid3 is a basal body protein required for the formation of primary cilia, an organelle involved in signal transduction. Here, we asked if Talpid3 has a role in the regulation of differentiation and/or self-renewal of ES cells and whether cells lacking cilia due to a deletion in Talpid3 can be reprogrammed to induced pluripotent stem (iPS) cells. We show that mouse embryonic limb fibroblasts which lack primary cilia with a targeted deletion in the <i>Talpid3</i> (<i>Ta3</i>) gene can be efficiently reprogrammed to iPS cells. Furthermore, vector-free <i>Ta3<sup>−/−</sup></i> iPS cells retain ES cell features and are able to self-renew. However, both <i>Ta3<sup>−/−</sup></i> iPS and ES cells are unable to form visceral endoderm and differentiate poorly into neurons. The observed defects are not a consequence of reprogramming since <i>Ta3<sup>−/−</sup></i> ES cells also exhibit this phenotype. Thus, Talpid3 and primary cilia are required for some differentiation events but appear to be dispensable for stem cell self-renewal and reprogramming. |
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| ISSN: | 2073-4409 |