The SCD5 Gene Modulates Adipogenic Differentiation via the WNT5B Signaling Pathway in Xinjiang Brown Cattle
by
, , , , , , and
Yiran Wang
,
Wanping Ren
,
Wei Shao
,
Yuxin Zhou
,
Yili Liu
,
Junwei Cao
,
Fengju Wang
,
Jingdong Bi
and
Liang Yang
* Xinjiang Herbivore Nutrition Laboratory for Meat & Milk, College of Animal Science, Xinjiang Agricultural University, No. 311 Nongda East Road, Urumqi 830052, China
*
Author to whom correspondence should be addressed.
Animals 2025, 15(24), 3547; https://doi.org/10.3390/ani15243547
Submission received: 29 October 2025
/
Revised: 30 November 2025
/
Accepted: 2 December 2025
/
Published: 10 December 2025
(This article belongs to the Special Issue Advances in Cattle Genetics and Breeding)
Simple Summary
The deposition of fat in beef cattle directly impacts meat yield and quality. To better understand the regulation of adipocyte (fat cell) development, this study focused on a gene called SCD5. We found that SCD5 acts as a “brake” in the formation of bovine fat cells: enhancing its activity slowed down the multiplication of fat cell precursors and their ability to store fat, whereas reducing its activity accelerated these processes. Further investigation into the mechanism revealed that SCD5 exerts this braking effect by suppressing a key signaling pathway known as WNT5B/β-catenin. In conclusion, our work identifies SCD5 as a crucial negative regulator of fat formation in cattle. This discovery provides new insights into the biology of fat deposition in livestock and suggests a novel target for future breeding strategies aimed at improving meat quality and yield.
Abstract
This study investigated the role of SCD5 in bovine preadipocyte proliferation and adipogenic differentiation. SCD5 overexpression suppressed proliferation, reducing the percentage of EdU-positive cells and overall cell viability (p < 0.05). It also downregulated proliferative factors CDK1 and CDK2 (p < 0.05), and reduced lipid accumulation (p < 0.001) along with key adipogenic markers PPARγ, C/EBPα, and FABP4 (p < 0.01). Conversely, SCD5 knockdown promoted these processes. Mechanistically, SCD5 overexpression downregulated WNT5B (p < 0.05), while knockdown had the opposite effect. Silencing WNT5B significantly decreased β-catenin transcription (p < 0.05), total protein (p < 0.05), and phosphorylation (p < 0.001). In conclusion, our findings identify SCD5 as a novel negative regulator of bovine preadipocyte proliferation and differentiation, which exerts its function through the WNT5B/β-catenin signaling axis. This discovery elucidates previously uncharacterized regulatory mechanisms underlying adipogenesis in livestock species.
Keywords:
SCD5; WNT5B pathway; preadipocyte; proliferation; adipogenic differentiation
