RESUMEN
Background: Cell confluency and serum deprivation promote the transition of C2C12 myoblasts into myocytes and subsequence fusion into myotubes. However, despite all myoblasts undergoing the same serum deprivation trigger, their responses vary: whether they become founder myocytes, remain proliferative, or evolve into fusion-competent myocytes remains unclear. We have previously shown that depletion of the scaffolding protein palladin in myoblasts inhibits cell migration and promotes premature muscle differentiation, pointing to its potential significance in muscle development and the necessity for a more in-depth examination of its function in cellular heterogeneity. Methods and results: Here, we showed that the subcellular localization of palladin might contribute to founder-fate cell decision in the early differentiation process. Depleting palladin in C2C12 myoblasts depleted integrin-ß3 plasma membrane localization of and focal adhesion formation at the early stage of myogenesis, decreased kindlin-2 and metavinculin expression during the myotube maturation process, leading to the inability of myocytes to fuse into preexisting mature myotubes. This aligns with previous findings where early differentiation into nascent myotubes occurred but compromised maturation. In contrast, wildtype C2C12 overexpressing the 140-kDa palladin isoform developed a polarized morphology with star-like structures toward other myoblasts. However, this behaviour was not observed in palladin-depleted cells, where the 140-kDa palladin overexpression could not recover cell migration capacity, suggesting other palladin isoforms are also needed to establish cell polarity. Conclusion: Our study identifies a counter-intuitive role for palladin in regulating myoblast-to-myocyte cell fate decisions and impacting their ability to form mature multinucleated myotubes by influencing cell signalling pathways and cytoskeletal organization, necessary for skeletal muscle regeneration and repair studies.
RESUMEN
This study presents a comprehensive assessment of persistent organic pollutants (POPs) in the blubber of a stranded blue whale found on the coast of Taiwan. The analysis included polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), dichlorodiphenyltrichloroethane (DDT), Hexachlorobenzene (HCB), and polybrominated diphenyl ethers (PBDEs). The whale exhibited evident signs of emaciation, including low body weight, reduced blubber fat content, and thin blubber thickness. The dominant fatty acid type detected in the blubber was short-chain monounsaturated fatty acids (SC-MUFA), known to aid in thermoregulation. Stable isotope ratios indicated that the blue whale occupied a lower trophic position compared to a fin whale, suggesting its proximity to krill habitats in the Southern Ocean for feeding. The average concentrations of DDTs (1089.2 ± 4.7 ng/g lw; ΣDDT) and PCBs (1057.1 ± 49.8 ng/g lw) in the blubber were almost one order of magnitude higher than PAHs (41.7 ± 10.0 ng/g lw), HCB (70.6 ± 2. ng/g lw), and PBDEs (7.2 ± 1.2 ng/g lw). Pollutant concentrations in this individual blue whale were comparable to levels found in Norway, higher than those found in Chile, and notably lower than those found in Canada and Mexico. Calculating the biomagnification factor (BMF) for the POPs from krill (Euphausia superba) to the blue whale revealed significant bioaccumulation of pollutants in this particular whale. Additional research is imperative to achieve a thorough comprehension of bioaccumulation of POPs and their potential toxicological impacts on whale health.