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Obesity is one of the dramatic health issues affecting developed and developing nations, and exercise is a well-established intervention strategy. While exercise-by-genotype interactions have been shown in humans, overall little is known. Using the natural negative geotaxis of Drosophila melanogaster, an important model organism for the study of genetic interactions, a novel exercise machine, the TreadWheel, can be used to shed light on this interaction. The mechanism for inducing exercise with the TreadWheel is inherently gentle, thus minimizing possible confounding effects of other stressors. Using this machine, we were able to assess large cohorts of adult flies from eight genetic lines for their response to exercise after one week of training. We measured their triglyceride, glycerol, protein, glycogen, glucose content, and body weight, as well as their climbing ability and feeding behavior in response to exercise. Exercised flies showed decreased stored triglycerides, glycogen, and body weight, and increased stored protein and climbing ability. In addition to demonstrating an overall effect of TreadWheel exercise on flies, we found significant interactions of exercise with genotype, sex, or genotype-by-sex effects for most of the measured phenotypes. We also observed interaction effects between exercise, genotype, and tissue (abdomen or thorax) for metabolite profiles, and those differences can be partially linked to innate differences in the flies' persistence in maintaining activity during exercise bouts. In addition, we assessed gene expression levels for a panel of 13 genes known to be associated with respiratory fitness and found that many responded to exercise. With this study, we have established the TreadWheel as a useful tool to study the effect of exercise in flies, shown significant genotype-specific and sex-specific impacts of exercise, and have laid the ground work for more extensive studies of how genetics, sex, environment, and aging interact with exercise to influence metabolic fitness in Drosophila., Competing Interests: The authors have declared that no competing interests exist.

Formation of mammalian skeletal muscle myofibers, that takes place during embryogenesis, muscle growth or regeneration, requires precise regulation of myoblast adhesion and fusion. There are few evidences showing that adhesion proteins play important role in both processes. To follow the function of these molecules in myoblast differentiation we analysed integrin alpha3, integrin beta1, ADAM12, CD9, CD81, M-cadherin, and VCAM-1 during muscle regeneration. We showed that increase in the expression of these proteins accompanies myoblast fusion and myotube formation in vivo. We also showed that during myoblast fusion in vitro integrin alpha3 associates with integrin beta1 and ADAM12, and also CD9 and CD81, but not with M-cadherin or VCAM-1. Moreover, we documented that experimental modification in the expression of integrin alpha3 lead to the modification of myoblast fusion in vitro. Underexpression of integrin alpha3 decreased myoblasts' ability to fuse. This phenomenon was not related to the modifications in the expression of other adhesion proteins, i.e. integrin beta1, CD9, CD81, ADAM12, M-cadherin, or VCAM-1. Apparently, aberrant expression only of one partner of multiprotein adhesion complexes necessary for myoblast fusion, in this case integrin alpha3, prevents its proper function. Summarizing, we demonstrated the importance of analysed adhesion proteins in myoblast fusion both in vivo and in vitro.

Objective: In this report, we demonstrate the participation of human cord blood (HUCB) stem cells in the skeletal muscle regeneration of SCID (severe combined immunodeficient) mice., Materials and Methods: The HUCB cells were labeled with the PKH26 fluorescent marker or recognized by an anti-HLA-ABC or anti-beta-2-microglobulin antibody. The HUCB cells were implanted directly into the damaged mouse muscle. The regeneration process and the implanted HUCB cells were traced each day after the damage, throughout a period of 7 days, and additionally at day 30 with the use of flow cytometry and confocal microscopy., Results: The PKH26-labeled cells isolated from the regenerating muscle were positive for the anti-HLA-ABC antibody. The percentage of the PKH26(+) and HLA-ABC(+) cells decreased from day 1 to day 5. In the regenerating muscle, the percentage of the HLA-ABC(+) cells increased, as measured on days 7 and 30. Moreover, myofibers containing fragments of the PKH26-labeled sarcolemma were noticed. Labeling with the anti-human beta(2)-microglobulin antibody showed the presence of positive cells and myofibers at day 7 of the regeneration, suggesting fusion of human and mouse cells., Conclusions: We suggest that the HUCB cells implanted into the damaged muscle are present there for at least 30 days and that they participate in the muscle regeneration. Moreover, our study shows that the implanted HUCB cells form human muscle precursor cells residing in the repaired mouse muscle. We suggest that the HUCB cell circulation after transplantation depends on SDF-1 (stromal-derived factor-1) expression in regenerating muscle.

Stem cells for skeletal muscle originate from dermomyotome of the embryo. The early marker of these cells is expression of both transcription factors Pax3 and Pax7 (Pax3+/Pax7+ cells). The skeletal muscles in the adult organism have a remarkable ability to regenerate. Skeletal muscle damage induces degenerative phase, followed by activation of inflammatory and satellite cells. The satellite cells are quiescent myogenic precursor cells located between the basal membrane and the sarcolemma of myofiber and they are characterized by Pax7 expression. Activation of the satellite cells is regulated by muscle growth and chemokines. Apart from the satellite cells, a population of adult stem cells (muscle side population--mSP) exists in the skeletal muscles. Moreover, the cells trafficking from different tissues may be involved in the regeneration of damaged muscle. Trafficking of cells in the process of damaged muscle regeneration may be traced in the SCID mice.

Protein kinase C (PKC) activity of cytosol and membrane fractions of 10T1/2 cells was studied. In cytosol of fast growing cells PKC activity was found in material eluted with 0.150 M NaCl whereas in membrane fractions activity was eluted with 0.065 and 0.150 M NaCl. In the membrane fraction of confluent cells, in contrast to cytosol, very low PKC activity was observed. The translocation pattern of PKC activity eluted with 0.065 M NaCl may be associated with proliferation.