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Many studies have reported that cyclin-dependent kinase inhibitor 3 (CDKN3) is involved in the cell cycle. However, the function of CDKN3 has not been well elucidated in organisms. In this study, a multiallelic indel caused by a 19-bp fragment and a 2 × 19 bp fragment was shown for the first time to be inserted into the promoter of the CDKN3 gene in 1994 chickens from 9 different breeds. In addition, 6 genotypes (C5C5, C4C4, C3C3, C4C5, C3C4, and C3C5) were observed (C3C3, C4C4, C5C5 have 3 × 19 bp, 4 × 19 bp, and 5 × 19 bp, respectively). Among these genotypes, the C4C4 genotype was the most dominant genotype in 9 breeds. The results of χ2 analysis of CDKN3 gene in different breeds showed that there were significant differences in the distribution of genotypes among different cultivars (P < 0.01). In addition, association study with F2 chicken resource population which produced by Anka and Gushi chickens showed that the C3C4 genotypes had the greatest semi-evisceration weight (SEW, 1163.94 ± 46.84), evisceration weight (EW, 964.15 ± 41.16), head weight (HW, 45.55 ± 1.43), claw weight (CW, 63.42±2.86), wing weight (WW, 129.15±5.48), liver weight (LW, 29.96±1.27), carcass weight (cW, 1286.96±49.53), weight at 10 (1190.68±45.68) and 12 (1430.65±54.45) wk, followed by C3C3, C4C4, C5C5, C4C5, whereas C3C5 genotypes having the lowest SEW (989.21±47.71), EW (841.38±40.55), HW (41.03±1.46), CW (54.36±2.81), WW (116.31±5.39), LW (27.31±1.25), cW (1093.29±49.99), weight at 10 (1036.10±44.99) and 12 (1246.28±53.59) wk. Expression levels of CDKN3 in breast muscle of chickens with C4C4 (0.72±0.02), C3C3 (0.95±0.41), and C4C5 (0.74±0.13) genotypes were significantly lower than those with C5C5 (1.80±0.01) and C3C5 (2.14±0.17) genotypes (P < 0.05). In conclusion, we investigated the effect of a multiallelic indel in the CDKN3 gene on the economic traits of chickens, and this indel was significantly associated with growth and carcass traits in chickens. Collectively, our findings provide useful information about the repeat sequence indel in the promoter region of the CDKN3 gene as a potential molecular marker for chicken breeding. [ABSTRACT FROM AUTHOR]

The high-yielding Houdan chicken (GGF) is characterized by high egg production and disease resistance. This study conducted whole genome resequencing of the GGF population and compared it to data from other breeds. Genetic diversity analysis revealed higher observed heterozygosity (Ho), Polymorphism information content (PIC), number of runs of homozygosity (ROH), and inbreeding coefficient (F ROH ) in GGF. Linkage disequilibrium (LD) decay was slowest in GGF, indicating intensive inbreeding and strong selection. These findings suggest a need for appropriate strategies to enhance genetic diversity conservation in this breed. Population structure analysis demonstrated that GGF was genetically distinct from both the red jungle fowl (RJF) and Chinese indigenous chicken (CIC) populations, highlighting GGF as a unique genetic resource warranting intensive protection and utilization. Selective sweep analysis identified genes under selection in GGF, primarily enriched in signaling pathways related to oocyte meiosis and progesterone-mediated oocyte maturation. Key candidate genes included: CCNE1, SKP1, CDC20, CDK2, ADCY8, RPS6KA6, PPP3CB, PDE3B, HSP90AB1, and AKT3. These findings provide a theoretical foundation for their potential application in poultry breeding. Additionally, this study combined bioinformatics analysis with PCR amplification and Sanger sequencing to identify 4 SNPs that can serve as a molecular identity card (ID) for GGF: SNP1 (Chr2: 136130976), SNP3 (Chr4:11705164), SNP4 (Chr4: 63255588), and SNP5 (Chr24: 3271008). This study provides a scientific basis for effective management and conservation of GGF genetic resources, and establishes a simple, economical, and accurate set of molecular IDs to combat the proliferation of inferior breeds and protect genetic resources., Competing Interests: DISCLOSURES The authors declare that they have no conflicts of interest., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)