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Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development

Although the conditional gene knockout (KO) is a better choice for observing its phenotype in a specific cell, tissue, and/or organ, the simple null gene KO could nevertheless be attempted initially to scan its overall phenotypes at the level of the whole-body system, especially for a new gene such...

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Autores principales: Choi, Seung-Young, Pi, Joo-Hyun, Jeong, So-Eun, Kang, Chang-Joong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8951461/
https://www.ncbi.nlm.nih.gov/pubmed/35328065
http://dx.doi.org/10.3390/genes13030511
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author Choi, Seung-Young
Pi, Joo-Hyun
Jeong, So-Eun
Kang, Chang-Joong
author_facet Choi, Seung-Young
Pi, Joo-Hyun
Jeong, So-Eun
Kang, Chang-Joong
author_sort Choi, Seung-Young
collection PubMed
description Although the conditional gene knockout (KO) is a better choice for observing its phenotype in a specific cell, tissue, and/or organ, the simple null gene KO could nevertheless be attempted initially to scan its overall phenotypes at the level of the whole-body system, especially for a new gene such as Crlz-1. Therefore, with a hope to glean phenotypic clues for Crlz-1 at the whole-body system, we attempted to generate its null KO mice. Contrary to our original desire, Crlz-1 homozygous null KO mice were not born. However, in the chasing of their homozygous KO embryos, they were found to be lethally impaired from early development, remaining in a state of small globular mass without ever leading to a body shape, indicating the critical role of Crlz-1 as a Wnt target gene for the proliferation and/or differentiation of cells during early mouse embryonic development.
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spelling pubmed-89514612022-03-26 Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development Choi, Seung-Young Pi, Joo-Hyun Jeong, So-Eun Kang, Chang-Joong Genes (Basel) Article Although the conditional gene knockout (KO) is a better choice for observing its phenotype in a specific cell, tissue, and/or organ, the simple null gene KO could nevertheless be attempted initially to scan its overall phenotypes at the level of the whole-body system, especially for a new gene such as Crlz-1. Therefore, with a hope to glean phenotypic clues for Crlz-1 at the whole-body system, we attempted to generate its null KO mice. Contrary to our original desire, Crlz-1 homozygous null KO mice were not born. However, in the chasing of their homozygous KO embryos, they were found to be lethally impaired from early development, remaining in a state of small globular mass without ever leading to a body shape, indicating the critical role of Crlz-1 as a Wnt target gene for the proliferation and/or differentiation of cells during early mouse embryonic development. MDPI 2022-03-14 /pmc/articles/PMC8951461/ /pubmed/35328065 http://dx.doi.org/10.3390/genes13030511 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Choi, Seung-Young
Pi, Joo-Hyun
Jeong, So-Eun
Kang, Chang-Joong
Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development
title Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development
title_full Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development
title_fullStr Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development
title_full_unstemmed Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development
title_short Crlz-1 Homozygous Null Knockout Mouse Embryos Are Lethally Stopped in Their Early Development
title_sort crlz-1 homozygous null knockout mouse embryos are lethally stopped in their early development
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8951461/
https://www.ncbi.nlm.nih.gov/pubmed/35328065
http://dx.doi.org/10.3390/genes13030511
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