Transcription factor Meis1b regulates craniofacial morphogenesis in zebrafish
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
LM2018124
Ministerstvo Školství, Mládeže a Tělovýchovy
LM2023050
Ministerstvo Školství, Mládeže a Tělovýchovy
LM2023052
Ministerstvo Školství, Mládeže a Tělovýchovy
RVO-68378050-KAV-NPUI
Ministerstvo Školství, Mládeže a Tělovýchovy
340321
Grantová Agentura, Univerzita Karlova
22-10660S
Grantová Agentura České Republiky
PubMed
39087648
DOI
10.1002/dvdy.731
Knihovny.cz E-zdroje
- Klíčová slova
- Meis, chondrocyte differentiation, craniofacial development, muscle fiber, zebrafish,
- MeSH
- chrupavka embryologie metabolismus MeSH
- crista neuralis embryologie metabolismus MeSH
- dánio pruhované * embryologie genetika MeSH
- homeodoménové proteiny * genetika metabolismus MeSH
- lebka * embryologie MeSH
- morfogeneze * genetika fyziologie MeSH
- mutace MeSH
- proteiny dánia pruhovaného * genetika metabolismus MeSH
- transkripční faktor Meis1 MeSH
- vývojová regulace genové exprese MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- homeodoménové proteiny * MeSH
- proteiny dánia pruhovaného * MeSH
- transkripční faktor Meis1 MeSH
BACKGROUND: Meis family of transcription factors operates in Pbx-Meis-Hox regulatory network controlling development of various tissues including eye, limbs, heart, hindbrain or craniofacial skeletal elements originating from the neural crest. Although studies in mouse provide abundant information about Meis factors function in embryogenesis, little is known about their role in zebrafish. RESULTS: We generated zebrafish lines carrying null mutations in meis1a, meis1b, meis2a, and meis2b genes. Only meis1b mutants are lethal at larval stage around 13 dpf whereas the other mutant lines are viable and fertile. We focused on development of neural crest-derived craniofacial structures such as tendons, cranial nerves, cartilage and accompanying muscles. Meis1b mutants displayed morphogenetic abnormalities in the cartilage originating from the first and second pharyngeal arches. Meckel's cartilage was shorter and wider with fused anterior symphysis and abnormal chondrocyte organization. This resulted in impaired tendons and muscle fiber connections while tenocyte development was not largely affected. CONCLUSIONS: Loss-of-function mutation in meis1b affects cartilage morphology in the lower jaw that leads to disrupted organization of muscles and tendons.
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