bioRxiv Science⌕ Search

bioRxiv · 10.1101/2024.09.20.614167

TBX15 regulates a network of immune response genes in adipose tissue and alters fat mass and depot weight in heterozygous knockout mice

Abstract

Adipose tissue distribution in the body is an indicator of metabolic disease risk, independent of body mass index (BMI), and is indirectly measured by waist-hip-ratio (WHR). T-Box transcription factor-15 (TBX15) has been implicated in regulation of adipose distribution in multiple human and mouse studies, and the TBX15-WARS2 genome-wide association study locus has been associated with BMI-adjusted-WHR signals in multiple investigations. As a potential mediator of this signal, we investigated the role of Tbx15 using heterozygous and homozygous mouse knockout models to determine if loss of this gene alters adipose physiology, and to identify the transcriptional network regulated by Tbx15 in adipose tissue and preadipocyte cells. In a metabolic phenotyping experiment we provided either low fat diet (LFD) or high fat diet (HFD) to male and female heterozygous Tbx15+/- and wildtype Tbx15+/+mice from weaning and maintained for 24 weeks. Only Tbx15+/-mice maintained on LFD weighed less than wildtype LFD controls, and female LFD Tbx15+/- mice had lower fat mass overall. We found that in LFD Tbx15+/- mice, multiple visceral fat depots weighed less than wildtype controls, and this was maintained when corrected for body mass for both gonadal and mesenteric visceral adipose depots. When comparing adipocyte size in multiple adipose depots, some reduction in number of larger adipocytes was detected in the perirenal adipose tissue of female HFD Tbx15+/- vs Tbx15+/+ mice, mesenteric adipose tissue from female LFD Tbx15+/- vs Tbx15+/+ mice and male HFD Tbx15+/- vs Tbx15+/+mice. RNA-sequencing of subcutaneous (inguinal) adipose tissues from 12-week old male and female knockout Tbx15-/-, Tbx15+/- and Tbx15+/+ mice raised on a standard chow diet identified 897 upregulated genes and 2328 downregulated genes in female Tbx15-/- mice compared to Tbx15+/+mice. We then combined this dataset with TBX15 ChIP-sequencing data from mouse preadipocyte 3T3-L1 cells overexpressing TBX15 to identify a credible set of genes directly regulated by TBX15. These 52 genes were enriched for B- and T-cell receptor signalling, JAK-STAT signalling and haematopoietic cell lineage pathways; suggesting a direct regulatory role for TBX15 in these pathways in adipose tissue. Together, these data highlight a role for TBX15 in regulation of differential adipose tissue expansion, particularly under low caloric conditions. Further, we identify a potentially important role for TBX15 in the well described adipocyte-immune cell crosstalk associated with obesity and type 2 diabetes mellitus.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Zolkiewski, L., Simon, M., Harrison, J., Vizor, L., Ireson, E., Moir, L., Yon, M. A., Beresford, L., Rodrigues, A., Hawkins, J., Hill, S., Bentley, L., Cox, R. D., Dumbell, R.. 2024-09-23. TBX15 regulates a network of immune response genes in adipose tissue and alters fat mass and depot weight in heterozygous knockout mice. https://doi.org/10.1101/2024.09.20.614167

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Hypothalamic Farnesoid X Receptor deficiency alters energy balance by modulating hepatic glucose production and adipose tissue metabolism through central insulin signaling.

Objectives: The bile acid nuclear receptor Farnesoid X Receptor (FXR, NR1H4) is a major regulator of metabolism and energy homeostasis in peripheral organs. It modulates bile acid, glucose, and lipid metabolism, as well as fat mass and body weight. However, FXR is also expressed in the brain, particularly in the hypothalamus, a key center for the regulation of energy homeostasis. Although one study has demonstrated a role for brain FXR activation in energy balance, its specific hypothalamic role is still unknown. Here, we examined the role of FXR in the mediobasal hypothalamus in the regulation of energy balance. Methods: We used a genetic approach combined with metabolic phenotyping to determine the effect of FXR invalidation in the mediobasal hypothalamus on metabolic parameters involved in the central regulation of energy homeostasis. Results: Our results demonstrate that hypothalamic FXR deficiency induces a positive energy balance, resulting in a reduction in energy expenditure due to alterations in glucose metabolism accompanied by structural changes in white adipose tissues. Conclusion: This study uncovers a previously unrecognized role for hypothalamic FXR in the central homeostatic control of energy balance, providing new insights into its contribution to peripheral glucose metabolism and adipose tissue structural remodeling.

physiology↗

Rad and Phospholamban are Key Drivers of the Ventricular Adrenergic Response and Stress-Induced Arrhythmia

The adrenergic response is a fundamental mechanism that regulates heart rate (chronotropy), cardiac contractility (inotropy) and relaxation (lusitropy). Adrenergic stress is also a recognized trigger of arrhythmia in disease. Yet, our understanding of the underlying molecular basis remains incomplete. Protein kinase A (PKA) and the calcium/calmodulin-dependent kinase II (CaMKII) phosphorylate multiple targets proposed to participate in the adrenergic response, including the GTP-binding protein Rad, phospholamban (PLB) and ryanodine receptor 2 (RyR2). Here we demonstrate that phosphorylation of both Rad and PLB is necessary for inotropy and lusitropy. We show that changes in cardiac contractility and relaxation are primarily dependent on intracellular calcium handling. Finally, we report that Rad and PLB control stress-induced arrhythmogenesis, despite the phosphorylation of other pro-arrhythmic targets. We have identified the essential molecular components of the adrenergic response, resolving a long-standing debate in cardiac excitation-contraction coupling and refining current models of sympathetic regulation in health and disease.

physiology↗

Light-cycle time-restricted feeding remodels a hidden layer of the cardiac transcriptome through sex-specific transcript switching

Light-cycle time-restricted feeding disrupts daily cardiovascular and thermoregulatory rhythms, but the molecular effects of light-cycle time-restricted feeding on the heart have been measured only at the level of total gene expression. We used Oxford Nanopore long-read RNA sequencing to resolve the full-length ventricular transcriptome from male and female mice under ad libitum feeding or light-cycle time-restricted feeding across the 24-hour cycle. Greater than 20% of cardiac transcripts represent unannotated variants of known genes absent from the current GENCODE reference annotation. Light-cycle time-restricted feeding reorganizes transcript usage across hundreds of genes, including genes encoding splicing regulators, largely without changing total gene expression. The genes affected are sex-specific, with fewer than 2% of changes shared at the gene, transcript, and transcript-usage levels. We show that transcript-level regulation is a previously underrecognized component of the cardiac response to altered feeding behavior, undetected by conventional short-read approaches.

physiology↗