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Consumers are increasingly demanding higher-quality mutton. Crossbreeding has been recognized as an effective means to improve meat quality. However, the phenomenon underlying these molecular system mechanisms remains largely unidentified. In this study, 48 male lambs aged 3 months were selected, including ♂ Hu sheep × ♀ Hu (HH, n = 16), ♂ Polled Dorset × ♀ Hu sheep F₁ hybrid lambs (DH, n = 16), and ♂ Southdown × ♀ Hu sheep (SH, n = 16) F₁ hybrid lambs, and raised in a single pen under the same nutritional and management conditions for 95 days. Then, seven sheep close to the average weight of the group were selected and fasted for 12 h prior to slaughter. By comparing the muscle fiber characteristics of the Longissimus dorsi of the three groups of sheep, and through transcriptomic and metabolomic analyses, we revealed molecular differences in the meat quality of Hu sheep crossbred with different parent breeds. The results of this study showed that muscle fiber diameter and cross-sectional area were significantly greater in the DH group than in the HH group, and collagen fiber content in the DH group was also significantly higher than in the HH group (p < 0.05). A total of 163 differential genes and 823 differential metabolites were identified in the three groups, most of which were related to muscle development and lipid metabolism. These included the AMPK signaling pathway, the PI3K-Akt signaling pathway, glycerophospholipid metabolism, and the related genes EFHB, PER3, and PPARGC1A. The results of this study offer valuable insights into the molecular mechanisms underlying the impact of crossbreeding on meat quality and provide a theoretical foundation for sheep crossbreed production. Full article

Breast cancer is among the most common malignancies in women. From the molecular point of view, breast cancer can be grouped into different categories, including the luminal (estrogen receptor positive (ER+)) and triple negative subtypes, which show distinctive features and, thus, are sensitive to different therapies. Breast cancer cells are strongly dependent on Ca²⁺ influx. Store-operated Ca²⁺ entry (SOCE) has been found to support a variety of cancer hallmarks including cell viability, proliferation, migration, and metastasis. The Ca²⁺ channels of the Orai family and the endoplasmic reticulum Ca²⁺ sensor STIM1 are the essential components of SOCE, but the extent of Ca²⁺ influx is fine-tuned by several regulatory proteins, such as the STIM1 modulators SARAF and EFHB. Here, we show that the expression and/or function of SARAF and EFHB is altered in breast cancer cells and both proteins are required for cell proliferation, migration, and viability. EFHB expression is upregulated in luminal and triple negative breast cancer (TNBC) cells and is essential for full SOCE in these cells. SARAF expression was found to be similar in breast cancer and pre-neoplastic breast epithelial cells, and SARAF knockdown was found to result in enhanced SOCE in pre-neoplastic and TNBC cells. Interestingly, silencing SARAF expression in ER+ MCF7 cells led to attenuation of SOCE, thus suggesting a distinctive role for SARAF in this cell type. Finally, we used a combination of approaches to show that molecular knockdown of SARAF and EFHB significantly attenuates the ability of breast cancer cells to proliferate and migrate, as well as cell viability. In aggregate, SARAF and EFHB are required for the fine modulation of SOCE in breast cancer cells and play an important role in the maintenance of proliferation, migration, and viability in these cells. Full article