A prominent example of seasonal phenotypic flexibility is the winter increase in thermogenic capacity （=summit metabolism, Msurn） in small birds, which is often accompanied by increases in pectoralis muscle mass and...A prominent example of seasonal phenotypic flexibility is the winter increase in thermogenic capacity （=summit metabolism, Msurn） in small birds, which is often accompanied by increases in pectoralis muscle mass and lipid catabolic capacity. Temperature or photoperiod may be drivers of the winter phenotype, but their relative impacts on muscle remodeling or lipid transport pathways are little known. We examined photoperiod and temperature effects on pectoralis muscle expres- sion of myostatin, a muscle growth inhibitor, and its tolloid-like protein activators （TLL-1 and TLL- 2）, and sarcolemmal and intracellular lipid transporters in dark-eyed juncos Junco hyemalis. We acclimated winter juncos to four temperature （3~C or 24~C） and photoperiod [short-day （SD） = 8L：16D; long-day （LD） = 16L：8D] treatments. We found that myostatin, TLL-I, TLL-2, and lipid transporter mRNA expression and myostatin protein expression did not differ among treatments, but treatments interacted to influence lipid transporter proteinexpression. Fatty acid translocase （FAT/CD36） levels were higher for cold SD than for other treatments. Membrane-bound fatty acid binding protein （FABPpm） levels, however, were higher for the cold LD treatment than for cold SD and warm LD treatments. Cytosolic fatty acid binding protein （FABPc） levels were higher on LD than on SD at 3℃, but higher on SD than on LD at 24℃. Cold temperature groups showed upregulation of these lipid transporters, which could contribute to elevated Msum compared to warm groups on the same photoperiod. However, interactions of temperature or photoperiod effects on muscle remodeling and lipid transport pathways suggest that these effects are context-dependent.展开更多
文摘A prominent example of seasonal phenotypic flexibility is the winter increase in thermogenic capacity （=summit metabolism, Msurn） in small birds, which is often accompanied by increases in pectoralis muscle mass and lipid catabolic capacity. Temperature or photoperiod may be drivers of the winter phenotype, but their relative impacts on muscle remodeling or lipid transport pathways are little known. We examined photoperiod and temperature effects on pectoralis muscle expres- sion of myostatin, a muscle growth inhibitor, and its tolloid-like protein activators （TLL-1 and TLL- 2）, and sarcolemmal and intracellular lipid transporters in dark-eyed juncos Junco hyemalis. We acclimated winter juncos to four temperature （3~C or 24~C） and photoperiod [short-day （SD） = 8L：16D; long-day （LD） = 16L：8D] treatments. We found that myostatin, TLL-I, TLL-2, and lipid transporter mRNA expression and myostatin protein expression did not differ among treatments, but treatments interacted to influence lipid transporter proteinexpression. Fatty acid translocase （FAT/CD36） levels were higher for cold SD than for other treatments. Membrane-bound fatty acid binding protein （FABPpm） levels, however, were higher for the cold LD treatment than for cold SD and warm LD treatments. Cytosolic fatty acid binding protein （FABPc） levels were higher on LD than on SD at 3℃, but higher on SD than on LD at 24℃. Cold temperature groups showed upregulation of these lipid transporters, which could contribute to elevated Msum compared to warm groups on the same photoperiod. However, interactions of temperature or photoperiod effects on muscle remodeling and lipid transport pathways suggest that these effects are context-dependent.
