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The effect of the timing of posthatch feed restriction on adipose deposition and adipogenic gene expression in the broiler pectoralis major muscle was studied by applying a 20% feed restriction either the first or second week after hatch. Broiler chicks at hatch were divided into a full-fed (control) group and a 20% feed restriction group. The expression of adipogenic genes, peroxisome proliferator-activated receptor gamma (PPARγ), and CCAAT/enhancer-binding protein alpha (C/EBPα) were measured. The expression of both PPARγ and C/EBPα was affected by the wk 1 feed restriction with expression significantly increased during the first week posthatch. The deposition of fat within the pectoralis major muscle was affected by the timing of the feed restriction. Extensive fat depots were present by 27 d of age in the pectoralis major muscle of the wk 1 restricted group compared with the control. Fat deposition was eliminated when the 20% feed restriction occurred in wk 2. Taken together, these results demonstrate that the timing of early posthatch feed restrictions in chicks is critical in the deposition of fat in the pectoralis major muscle and expression of adipogenic genes., (©2014 Poultry Science Association Inc.)

The effect of the timing of an immediate posthatch feed restriction on broiler pectoralis major muscle development was studied by applying a 20% feed restriction either the first or second week after hatch. Pectoralis major muscle morphological structure and the expression of the myogenic transcriptional regulatory factors, myogenic determination factor 1 (MyoD), myogenic regulatory factor 4 (MRF4), and myogenin, were measured. Broiler chicks at hatch were divided into a full-fed (control) group and a 20% feed restriction treatment administered either the first or second week posthatch. At the end of the feed restriction, the chicks were placed on a full feed ad libitum diet with no further restrictions. Muscle fiber diameter and fiber bundle size of the pectoralis major muscle were smaller in the wk 1 restricted group than the control group by 7 d of age. By 15 d of age through the duration of the study, d 43, both endomysial and perimysial connective tissue spacing were diminished in the wk 1 feed-restricted group. The expression of MyoD, MRF4, and myogenin was affected by the wk 1 feed restriction. The expression of MyoD and MRF4 was significantly increased during the first week posthatch. Both of the genes have been shown to be expressed during proliferation especially MyoD, which is required for muscle cell proliferation. In contrast, myogenin expression was significantly decreased. Myogenin expression is required for differentiation to occur. The morphological changes and gene expression changes observed with the wk 1 feed restriction were eliminated by moving the 20% feed restriction to wk 2, which is after the period of maximal myogenic satellite cell mitotic activity. Taken together, these results demonstrate that the timing of early posthatch feed restrictions to chicks is critical for the morphological development of the pectoralis major muscle and the expression of genes required for muscle satellite cell proliferation and differentiation., (Poultry Science Association Inc.)

The low score normal (LSN) chicken exhibits a genetic muscle weakness and altered in vitro myogenesis compared to the normal White Leghorn chicken. The ventricular myosin heavy chain isoform has been reported to be the initial muscle-specific contractile protein expressed during myogenesis. The goals of this study were to determine whether altered myogenesis of the LSN satellite cells in culture was accompanied by delayed ventricular myosin heavy chain expression and to further characterize the altered myogenic events exhibited by the LSN chicken. Immunocytochemical and ELISA analyses were employed to document the temporal expression of the ventricular myosin heavy chain during LSN chicken myogenesis. Satellite cells derived from the LSN chicken pectoralis major exhibited lower (P

Skeletal muscle development is, in part, regulated by myoblast-extracellular matrix interactions mediated by the transmembrane integrin family of heterodimeric receptors. The avian genetic muscle weakness, low score normal (LSN), exhibits modified myotube and sarcomere structure that may be associated with altered integrin expression. Protein expression of the beta1 integrin subunit was measured during normal and LSN Pectoralis major muscle development at 14, 16, and 18 d of embryonic development, and 1 d and 1 and 6 wk posthatch. During embryonic development, integrin expression was downregulated. However, by 1 wk posthatch, integrin levels were upregulated and remained elevated through 6 wk posthatch. This pattern was observed in both normal and LSN muscle development. Overall, beta1 integrin levels were lower in the LSN P. major muscle. In normal and LSN satellite cell cultures, beta1 integrin expression was low during proliferation. In early differentiation, beta1 integrin expression increased and was then downregulated. As observed in the muscle extracts, LSN beta1 integrin expression was significantly lower during differentiation. These results suggest that the regulation of beta1 integrin expression is critical to the progression of myogenesis, and, during LSN myogenesis, decreased expression of beta1 integrin may be associated with modifications in muscle structure.

The avian Low Score Normal (LSN) genetic muscle weakness is phenotypically characterized by a reduction in the ability of birds to right themselves from a supine position. In previous studies, LSN birds exhibited elevated levels of decorin transcript and protein at embryonic Day 20 and a large increase in collagen crosslinking at 6 wk posthatch. Transforming growth factor-beta (TGF-beta) expression has been reported to control decorin expression. Steady state levels of TGF-beta1 and TGF-beta2 transcripts were determined in ovo and posthatch in order to initiate an investigation of the mechanism underlying decorin expression. On embryonic Day 20 through 1 wk posthatch, TGF-beta2 transcript levels were elevated, whereas an increase in TGF-beta1 was only noted at 1 d posthatch. These data suggest that the increase in decorin expression may be associated with a modification in a TGF-beta signal transduction pathway.

The avian Low Score Normal (LSN) genetic muscle weakness is phenotypically characterized by a reduction in the ability of the birds to right themselves from a supine position. Compared to normal skeletal muscle, LSN muscle has normal myosin isoform switching and cell-cell recognition, elevated glycosaminoglycan and decorin levels at embryonic Day 20, and a large increase in collagen crosslinking at 6 wk posthatch. To begin to determine the biological mechanism involved in the elevated decorin protein concentration at embryonic Day 20, the steady-state levels of transcripts encoding both decorin and collagen Type I at embryonic Days 14, 19, and 20, and at 1 d and 6 wk posthatch were measured. On embryonic Day 20, collagen Type I transcripts were not different from the control but there was a significant elevation in decorin transcript levels. At 1 d and 6 wk posthatch, transcript levels of decorin and collagen Type I were not different between LSN and controls. The change in decorin transcript steady-state levels is limited to late embryonic development and suggests an alteration in a signal transduction pathway regulating decorin transcription.