In this study, we examined correlations between the deposition of inosine monophosphate (IMP) and mRNA expression of the adenylate kinase 1 (AK1) gene in Jingyuan chicken. The IMP content was determined by high-performance liquid chromatography. Transcriptome sequencing was used to screen the differentially expressed gene AK1 and real-time quantitative polymerase chain reaction (PCR) to determine the expression level of AK1 mRNA associated with IMP synthesis. IMP and inosine content in the breast muscles of both Jingyuan cocks and hens was found to be significantly higher than that in the leg muscles. Similarly, the expression of AK1 mRNA in the breast muscles of cocks and hens was significantly higher than that in the leg muscles. Moreover, AK1 mRNA expression in cock breast muscles was negatively correlated with IMP content, whereas its expression in cock leg muscles was positively correlated with IMP content. In contrast, the expression of AK1 mRNA in hen breast and leg muscles was significantly positively correlated with IMP content. These findings provide a scientific basis for enhancing the meat flavor of Jingyuan chicken and promoting the development and utilization of local variety resources, as well as constituting a basis for screening IMP-regulated genes. Our study will advance our current understanding of AK1 function.

N⁶-methyladenosine (m⁶A) is a critical epigenetic modification that regulates lipid metabolism; however, its role in adipogenesis in chickens remains unclear. Here, we demonstrated that the m⁶A methylase METTL3 shows significant differences at the key stage of chicken development, and its expression in the breast muscle is significantly higher than in other tissues. Furthermore, METTL3 expression gradually decreases during the differentiation of both intramuscular preadipocytes (IMPA) and abdominal preadipocytes (APA). Gain- and loss-of-function assays demonstrated that METTL3 overexpression significantly inhibited the proliferation and differentiation of IMPA and APA cells, whereas METTL3 knockdown exerted the opposite effect. Combined with m⁶A sequencing (m⁶A-seq), we identified significant enrichment of m⁶A modification within the 3' untranslated region (3'UTR) of PCYT1A mRNA, indicating it as a direct modification target of METTL3. Mechanistically, METTL3 knockdown reduced m⁶A methylation of PCYT1A, consequently enhancing PCYT1A mRNA stability and expression. This upregulation of PCYT1A promoted adipogenic differentiation in both IMPA and APA. Our study elucidates the functional mechanism by which METTL3-mediated m⁶A modification regulates lipid deposition through modulating PCYT1A expression, thereby identifying novel molecular targets for investigating adipogenesis in chickens.