Background: Cultivated meat, an alternative to conventional meat, has substantial potential for alleviating environmental and ethical concerns. This method of manufacturing meat involves the isolation of skeletal muscle satellite cells (SMSCs) from donor animals, after which they proliferate in vitro and differentiate into primitive muscle fibers. The aim of this research was to evaluate how the insulin-like growth factor 1 (IGF1) gene regulates the myogenic differentiation of bovine skeletal muscle satellite cells (bSMSCs). Methods: bSMSCs isolated from newborn calves were cultured to the third generation in vitro and differentiated into myoblasts via the serum withdrawal method. An overexpression lentivirus and siRNA targeting the IGF1 gene were constructed and transduced into bSMSCs, which were subsequently analyzed via real-time fluorescence quantitative PCR(qRT–PCR) and Western blots. The mRNA and protein levels of the myogenic differentiation markers myosin heavy chain (MyHC) and myogenin (MyoG) were determined. Results: The results revealed that the lentivirus overexpressing the IGF1 gene significantly increased the expression of MyHC and MyoG, whereas the expression of both the MyHC and MyoG mRNAs and proteins was strongly reduced by si-IGF1. Conclusions: IGF1 positively regulates the myogenic differentiation of bSMSCs. This study provides a reference for further elucidating the molecular mechanism by which the IGF1 gene regulates the myogenic differentiation of bSMSCs via the PI3K/Akt signaling pathway and lays a foundation for establishing a regulatory network of bovine muscle growth and development.

Fibroblast growth factor 9 (FGF9) is crucial for the growth and development of hair follicles (HFs); however, its role in sheep wool growth is unknown. Here, we clarified the role of FGF9 in HF growth in the small-tailed Han sheep by quantifying FGF9 expression in skin tissue sections collected at different periods. Moreover, we evaluated the effects of FGF9 protein supplementation on hair shaft growth in vitro and FGF9 knockdown on cultured dermal papilla cells (DPCs). The relationship between FGF9 and the Wnt/β-catenin signaling pathway was examined, and the underlying mechanisms of FGF9-mediated DPC proliferation were investigated. The results show that FGF9 expression varies throughout the HF cycle and participates in wool growth. The proliferation rate and cell cycle of FGF9-treated DPCs substantially increase compared to that of the control group, and the mRNA and protein expression of CTNNB1, a Wnt/β-catenin signaling pathway marker gene, is considerably lower than that in the control group. The opposite occurs in FGF9-knockdown DPCs. Moreover, other signaling pathways are enriched in the FGF9-treated group. In conclusion, FGF9 accelerates the proliferation and cell cycle of DPCs and may regulate HF growth and development through the Wnt/β-catenin signaling pathway.

Histone deacetylase 9 (HDAC9) is a histone deacetylase (HDAC) subtype IIa protein that deacetylates histone 3 (H3), histone 4 (H4), and nonhistone proteins in vivo to alter chromosomal shape and regulate gene transcription. There have been few studies on the regulatory influence of the HDAC9 gene on the differentiation of chicken embryonic stem cells (cESCs) into male germ cells, and the significance of HDAC9 is still unknown. Therefore, we explored the specific role of HDAC9 during differentiation of the cESCs of Jilin Luhua chickens through inhibition or overexpression. In medium supplemented with 10^-5 mol/L retinoic acid (RA), cESCs were stimulated to develop into germ cells. HDAC9 and germline marker gene mRNA and protein levels were measured using qRT‒PCR and western blotting. During the differentiation of cESCs into male germ cells, overexpression of the HDAC9 gene greatly increased the mRNA and protein expression levels of the germline marker genes Stra8, Dazl, c-kit, and integrin ɑ6. The HDAC9 inhibitor TMP195 significantly decreased the mRNA and protein expression levels of the above markers. In summary, HDAC9 positively regulates the differentiation of cESCs.