ArticleCommunications biology2020
Combined deletions of IHH and NHEJ1 cause chondrodystrophy and embryonic lethality in the Creeper chicken.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- A heterozygous deletion and inversion at the NHEJ1‑IHH locus associated with shank length in Yunlong short-leg chicken.BMC genomics · 2026Article
- A review of genetic variation underlying chicken phenotypic diversity.Poultry science · 2025Review
- Current Status and Prospects of Genetic Resources of Native Chickens of Japan.Animals : an open access journal from MDPI · 2025Review
- PGC-based cryobanking, regeneration through germline chimera mating, and CRISPR/Cas9-mediated TYRP1 modification in indigenous Chinese chickens.Communications biology · 2024Article
- Mycobacterial CpsA activates type I IFN signaling in macrophages via cGAS-mediated pathway.iScience · 2024Article
- Molecular cloning, subcellular localization, and rapid recruitment to DNA damage sites of chicken Ku70.Scientific reports · 2024Article
- Article
- Feline XRCC4 undergoes rapid Ku-dependent recruitment to DNA damage sites.FEBS open bio · 2022Article
- A genome-wide scan to identify signatures of selection in two Iranian indigenous chicken ecotypes.Genetics, selection, evolution : GSE · 2021Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Creeper (Cp) chicken is characterized by chondrodystrophy in Cp/+ heterozygotes and embryonic lethality in Cp/Cp homozygotes. However, the genes underlying the phenotypes have not been fully known. Here, we show that a 25 kb deletion on chromosome 7, which contains the Indian hedgehog (IHH) and non-homologous end-joining factor 1 (NHEJ1) genes, is responsible for the Cp trait in Japanese bantam chickens. IHH is essential for chondrocyte maturation and is downregulated in the Cp/+ embryos and completely lost in the Cp/Cp embryos. This indicates that chondrodystrophy is caused by the loss of IHH and that chondrocyte maturation is delayed in Cp/+ heterozygotes. The Cp/Cp homozygotes exhibit impaired DNA double-strand break (DSB) repair due to the loss of NHEJ1, resulting in DSB accumulation in the vascular and nervous systems, which leads to apoptosis and early embryonic death.
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