Background: The homologous proteins identified as cellular retinoic acid-binding proteins I and II (CRABP-I and CRABP-II) belong to a subset of intracellular proteins characterized by their robust affinity for retinoic acid, which plays an indispensable role in the development of hair follicle, including differentiation, proliferation, and apoptosis in keratinocytes. Previous research on Hu sheep hair follicles revealed the specific expression CRABP1 in dermal papilla cells (DPCs), suggesting that CRABP1 has a potential role in regulating the DPC population. Therefore, the main purpose of this study is to expose the performance of the CRABP1 genes in the development and proliferation of DPCs. Methods: Initially, overexpression and inhibition of CRABP1 in the DPCs were conducted through overexpression vector and siRNA. CCK-8, EDU, and RT-PCR cell cycle assays and immunostaining were performed to evaluate the proliferation and cell cycle of dermal papilla cells (DPCs). Although, the influence of CRABP1 upon β-catenin in dermal papilla cells (DPCs) was found using immunofluorescence labeling. Finally, RT-PCR was conducted to assess the impact of CRABP1 on the expression levels of CTNNB1, TCF4, and LEF1 in DPCs involved in the Wnt/β-catenin signaling pathway. Results: The results showed that CRABP1 overexpression promotes the growth rates of DPCs and significantly enhances the proportion of S-phase cells compared with the control group (p < 0.05). The results were the opposite when CRABP1 was a knockdown. In contrast, there was a significant decline in the mRNA expression levels of CTNNβ1, LEF1 (p < 0.05), and TCF4 (p < 0.01) by CRABP1 knockdown. Conclusions: This study found that CRABP1 influences the expression of important genes within the Wnt/β-catenin signaling pathway and promotes DPC proliferation. This investigation provides a theoretical framework to explain the mechanisms that control hair follicle morphogenesis and development.

Previous studies have indicated that changes in LYPLA1 expression affect the proliferation and differentiation of fetal sheep myoblasts; however, the underlying molecular mechanisms remain unclear. This study examined transcriptional responses to LYPLA1 overexpression and knockdown in primary myoblasts derived from one Hu sheep fetus and explored the involvement of PI3K-Akt signaling in LYPLA1-associated proliferation. RNA sequencing showed that no differentially expressed genes remained significant after false discovery rate correction following LYPLA1 knockdown, whereas LYPLA1 overexpression yielded 362 significant genes, including 219 upregulated and 143 downregulated genes. Exploratory enrichment analysis of nominally significant candidate genes implicated extracellular and immune-related functions, steroid hormone biosynthesis, PPAR signaling, cytokine–cytokine receptor interaction, and PI3K-Akt signaling. Pharmacological inhibition with 0.5 μM PI3K/AKT-IN-1 partially attenuated the increases in EdU-positive cells and Cyclin D1 mRNA levels associated with LYPLA1 overexpression. These findings indicate that LYPLA1 overexpression is associated with broad transcriptional changes in ovine myoblasts and suggest that PI3K-Akt signaling contributes to the associated proliferative phenotype. However, the underlying mechanism requires further validation.

Multi-parity records improve ewe evaluation but require long-term follow-up. This study compared litter size, litter weight, and lambing type across four parities in 256 Hu sheep and 90 Tan sheep and evaluated six candidate SNPs in Hu sheep. The SNPs were confirmed by PCR and Sanger sequencing and genotyped using PARMS; repeated records were analyzed with mixed-effects models. The Hu sheep population showed higher litter weight and multiple-birth proportions than the Tan sheep population, together with a higher mean litter size. Analysis of 822 records from 256 Hu ewes showed that both traits increased from the first to the third parity and then remained stable; the same pattern occurred in 156 ewes with complete records. After BH-FDR correction, BMPR1B rs418841713 and TSHR rs406686139 were significantly associated with both traits. Association directions were unchanged when analyses were restricted to complete records, low-frequency genotypes were recoded, or lambing year was included. In an independent population, combined-genotype differences were nonsignificant, although GGCG had the numerically highest total litter size. An exploratory model indicated that first-parity litter size and both genotypes provided information on subsequent litter weight, but predictive performance was limited. These findings support further validation of BMPR1B and TSHR in Hu sheep.

Lambing interval is an indicator of reproductive efficiency in ewes. This study characterized population-level lambing interval patterns in Hu and Tan sheep and evaluated three previously reported candidate SNPs in ADAMTSL1, CD226, and PAPPA. Among 256 genotyped Hu ewes and 94 genotyped Tan ewes, 244 and 92 ewes, respectively, had at least two valid lambing dates. After applying a unified quality-control range of 180–450 days, 711 intervals from 230 Hu ewes and 219 intervals from 82 Tan ewes were retained. The raw mean lambing intervals were 277.81 ± 27.56 days in Hu sheep and 368.81 ± 22.51 days in Tan sheep. After adjustment for parity, year, season, preceding litter size, and repeated ewe records, Tan sheep had an 80.99-day longer interval than Hu sheep (95% CI: 75.34–86.64 days; p = 3.17 × 10⁻¹²⁶). This difference remained significant across all parity groups. None of the three candidate SNPs was significantly associated with adjusted lambing interval after false-discovery-rate correction. Analyses of within-ewe interval variability also yielded no supported associations, although CD226 showed a weak, non-significant tendency toward lower variability in Hu sheep. These findings demonstrate a marked population-level difference in reproductive timing but do not support the immediate use of the tested SNPs as markers for lambing interval or within-ewe interval variability.