Background: The interplay between the gut microbiome and host physiology is a critical determinant of health and metabolism, particularly within the gut-muscle axis. While correlations between specific bacterial taxa and host gene expression are known, the specific transcription factors (TFs) orchestrating these molecular responses in skeletal muscle remain largely uncharacterized. Identifying these key regulators is crucial to understanding the mechanisms linking gut ecology to host phenotype. Aim: This study aimed to identify key TFs that potentially regulate a co-expressed gene network in porcine skeletal muscle associated with the abundance of specific cecal bacterial genera. Methodology: Skeletal muscle transcriptomic (RNA-Seq, ~14k expressed genes as TPM counts) and cecal microbiome (16S rRNA) data were obtained from 32 male castrated Large White pigs. Weighted Gene Co-expression Network Analysis (WGCNA) in R was used to identify co-expression modules, which were then correlated with the top ten most abundant bacterial genera. Genes from the most relevant module were subjected to a TF enrichment analysis using the ChEA 2022 library from the Enrichr platform. Results: WGCNA identified 12 gene modules. We highlight the MEyellow module (720 genes), which correlated with three of the four most abundant cecal genera: positively with Clostridium (r=0.34) and Romboutsia (r=0.31), and negatively with Ruminococcaceae UCG-005 (r=-0.37). Enrichment analysis of this module revealed a highly significant over-representation of targets for master TFs, including RUNX Family Transcription Factor 2 (RUNX2; Adjusted P-value=2.60E-25), Vitamin D Receptor (VDR; Adjusted P-value=5.17E-20), and YY1 Transcription Factor (YY1; Adjusted P-value=2.27E-23), all known regulators of cellular development and metabolism. Conclusion: Abundant gut bacteria are linked to a distinct muscle transcriptional program in pigs: the TFs RUNX2 and VDR form a mechanistic bridge between the gut microbiome and the host's muscular response, defining a novel regulatory axis.