1. We hypothesise that administration of available glutamine and carbohydrates by in ovo injection may provide energy for small intestine and duck embryo activity, in turn alleviating energy lack, sparing the pectoralis muscle protein and increasing breast muscle mass. To test this hypothesis, 220 duck eggs at 21 d of incubation were chosen and assigned to two treatments. At 23 d of incubation, glutamine, digestible sucrose and maltose were injected into the amniotic fluid in the treatment group. 2. In ovo injection of glutamine and carbohydrates improved small intestine development, as reflected in the increase in weight and sucrase activity, though gizzard, proventriculus and liver weight were not affected by the in ovo injection. 3. Compared with control, pectoralis weight in treatment ducks was increased by 24% at 25 d of incubation and 15% at hatch and this advantage was sustained until 7 d posthatch. In ovo injection improved duck weight gain in the early days posthatch. 4. The results of the present study suggest that in ovo injection of glutamine and carbohydrates improves small intestine development and pectoralis mass, which is probably due to sparing of breast muscle protein.

The SRF/MRTF and upstream signaling cascade play key roles in actin cytoskeleton organization and myocyte development. To date, how this signaling axis may function in brown adipocyte lineage commitment and maturation has not been delineated. Here we report that MRTF-SRF signaling exerts inhibitory actions on brown adipogenesis, and suppressing this negative regulation promotes brown adipocyte lineage development. During brown adipogenic differentiation, protein expressions of SRF, MRTFA/B and its transcription targets were down-regulated, and MRTFA/B shuttled from nucleus to cytoplasm. Silencing of SRF or MRTF-A/MRTF-B enhanced two distinct stages of brown adipocyte development, mesenchymal stem cell determination to brown adipocytes and terminal differentiation of brown adipogenic progenitors. We further demonstrate that the MRTF-SRF axis exerts transcriptional regulations of the TGF-β and BMP signaling pathway, critical developmental cues for brown adipocyte development. TGF-β signaling activity was significantly attenuated, whereas that of the BMP pathway augmented by inhibition of SRF or MRTF-A/MRTF-B, leading to enhanced brown adipocyte differentiation. Our study demonstrates the MRTF-SRF transcriptional cascade as a negative regulator of brown adipogenesis, through its transcriptional control of the TGF-β/BMP signaling pathways.

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The circadian clock is entrained to daily environmental cues. Integrin-linked signaling via actin cytoskeleton dynamics transduces extracellular matrix physical niche cues to Myocardin-related Transcription Factor (MRTF)/Serum Response Factor (SRF)-mediated transcription. Actin cytoskeleton organization and SRF-MRTF activity displays diurnal oscillations. By interrogating disparate upstream events in actin cytoskeleton-MRTF-A/SRF signaling cascade, here we show that this pathway transduces extracellular niche cues to modulate circadian clock function. Pharmacological inhibitions of MRTF-A/SRF, by disrupting actin polymerization or blocking ROCK kinase, induced period lengthening with augmented clock amplitude, and genetic loss-of-functions of Srf or Mrtf-a mimic that of actin-depolymerizing agents. In contrast, actin polymerization shortened circadian clock period with attenuated amplitude. Moreover, interfering with cell-matrix interaction through blockade of integrin, inhibition of focal adhesion kinase or attenuating matrix rigidity reduced period length while enhancing amplitude. Mechanistically, we identify that core clock repressors, Per2, Nr1d1, and Nfil3, are direct transcriptional targets of MRTF-A/SRF in mediating actin dynamic-induced clock response. Collectively, our findings defined an integrin-actin cytoskeleton-MRTF/SRF pathway in linking clock entrainment with extracellular cues that may facilitate cellular adaptation to its physical niche environment.

No abstract