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Jesse N Weber

Publications and source records attributed to Jesse N Weber.

2 recordsLinked to original sources

A spectral framework to map QTLs affecting joint differential networks of gene co-expression.

Studying the mechanisms underlying the genotype-phenotype association is crucial in genetics. Gene expression studies have deepened our understanding of the genotype  →  expression  →  phenotype mechanisms. However, traditional expression quantitative trait loci (eQTL) methods often overlook the critical role of gene co-expression networks in translating genotype into phenotype. This gap highlights the need for more powerful statistical methods to analyze genotype  →  network  →  phenotype mechanism. Here, we develop a network-based method, called spectral network quantitative trait loci analysis (snQTL), to map quantitative trait loci affecting gene co-expression networks. Our approach tests the association between genotypes and joint differential networks of gene co-expression via a tensor-based spectral statistics, thereby overcoming the ubiquitous multiple testing challenges in existing methods. We demonstrate the effectiveness of snQTL in the analysis of three-spined stickleback (Gasterosteus aculeatus) data. Compared to conventional methods, our method snQTL uncovers chromosomal regions affecting gene co-expression networks, including one strong candidate gene that would have been missed by traditional eQTL analyses. Our framework suggests the limitation of current approaches and offers a powerful network-based tool for functional loci discoveries.

Quantitative Trait Loci↗

Myocyte enhancer factor-2 and serum response factor binding elements regulate fast Myosin heavy chain transcription in vivo.

Adult fast muscle fibers express distinct myosin heavy chains (MyHC) in differing proportions, but the mechanisms underlying their differential expression remain undefined. We used a variety of in vitro and in vivo approaches to explore the contribution of transcriptional regulation to adult fast MyHC expression. Here we show that 800-1000 bp of a sequence upstream of the three mouse adult fast MyHC genes (Ia, IIb, and IId/x) are sufficient to drive muscle-specific and fiber-specific expression in vivo. We show that the upstream promoter region of the gene most abundantly expressed in mouse skeletal muscles, IIb MyHC, retains binding activity and transcriptional activation for three positive transcription factors, the serum response factor, Oct-1, and myocyte enhancer factor-2, whereas the other two genes (IIa and IId/x) have nucleotide substitutions in these sites that reduce binding and transcriptional activation. Finally, we demonstrate that regions upstream of 300 bp modulate the effects of these elements. Together, these data demonstrate that the quantitative differences in MyHC expression in mouse skeletal muscle have evolved at least in part through the elimination of positive-acting transcription factor binding sites.

Animals↗