The effect of posthatch starvation on skeletal muscle growth and satellite cell proliferation was examined in chicks. Chicks were either fed or starved for 48 h posthatch (d 0-d 2, d 2-d 4 or d 4-d 6) and then refed for 41 d. Body and breast muscle weights were significantly lower in starved chicks than in fed controls throughout the experiment. Histochemical staining revealed that skeletal muscle fiber development in the starved group lagged behind that of the fed group. Starvation from d 2 to 4 and d 4 to 6 posthatch had a progressively lesser effect than did immediate posthatch starvation (P < 0.05). In vitro culturing of breast muscle satellite cells revealed that DNA synthesis and number of cells per gram of muscle in the fed chicks peaked on d 2 and d 3, and then declined. In contrast, DNA synthesis in the cells of starved chicks declined on d 2 and increased on d 3 when chicks were refed. A similar pattern was seen for the number of cells per gram muscle; however, in general cell numbers tended to be higher in the starved group than in controls (P < 0.1). The results obtained with cultured cells were parallel with in situ immunostaining with 5-bromo-2'-deoxyuridine and proliferating cell nuclear antigen in breast muscle from experimental chicks, and with growth hormone receptor expression. These results suggest that satellite cell cultures are a reliable tool for evaluating muscle growth in postnatal chickens. We conclude that sufficient feed in the immediate postnatal period is critical for satellite cell proliferation and skeletal muscle development and is thus important for optimal muscle growth.

Changes in the morphology of the small intestinal mucosa and enterocyte dynamics were examined in posthatch chicks through 12 d. At hatch, enterocytes were round and nonpolar; however, within 24 h posthatch, enterocytes lengthened and exhibited more typical morphology. Crypts were rudimentary at hatch and by 48 h invagination was completed and crypt numbers increased by branching and fission, with the number of crypts per villus reaching plateau after 72 h posthatch. All epithelial cells were proliferative at hatch. In the crypts, the proportion of proliferating enterocytes decreased to 50 to 60% within 2 d posthatch, whereas along the villus the proportion of proliferating cells decreased to 10 to 20% by 6 d. Different patterns of temporal development of villi were observed in the duodenum, jejunum and ileum. Individual villus surface area increased steadily in the duodenum throughout the experiment, whereas individual jejunal and ileal villus surface areas increased more slowly after 4 d posthatch. The number of villi per cross-section of intestine increased in the duodenum and jejunum but not in the ileum. The total segment villus surface area increased similarly in all segments until 3 d posthatch, after which the jejunum increased considerably in absorptive area, whereas the duodenum and ileum increased more slowly. This study shows that, in the hatching chick, the small intestine matures in a manner similar to neonatal mammals, with specific ontogenetic timetables in the different small intestinal segments, however, the most dramatic changes occur within the first 24 h posthatch.

Skeletal myogenesis is controlled by bHLH transcription factors of the MyoD family that, along with MEF-2 factors, comprise a positive feedback network that maintains the myogenic transcriptional program. Cell-cell contact between muscle precursors promotes myogenesis, but little is known of the underlying mechanisms. CDO, an Ig superfamily member, is a component of a cell surface receptor complex found at sites of cell-cell contact that positively regulates myogenesis in vitro. We report here that mice lacking CDO display delayed skeletal muscle development. Additionally, satellite cells from these mice differentiate defectively in vitro. CDO functions to activate myogenic bHLH factors via enhanced heterodimer formation, most likely by inducing hyperphosphorylation of E proteins. The Cdo gene is, in turn, a target of MyoD. The promyogenic effect of cell-cell contact is therefore linked to the activity of myogenic bHLH factors. Furthermore, the myogenic positive feedback network extends from the cell surface to the nucleus.

The small intestines of hatching chicks undergo rapid developmental changes in the immediate post-hatch period when the birds are making the transition from endogenous nutrient supply from yolk to dependence on exogenous feed. This transition usually only begins 48 h or more after hatching, owing to logistical considerations of production. The effects of fasting for 48 h at different times during this critical period on small intestinal development and enterocyte dynamics were examined by morphometric determinations and use of staining for proliferative-cell nuclear antigen and 5-bromo-2-deoxyuridine. The effects of fasting were specific to both time of fasting and the intestinal segment examined. Decreased development was found in the duodenum and jejunum, but was less apparent in the ileum. Fasting between 0 and 48 h decreased crypt size in the duodenum and jejunum, the number of crypts per villus, crypt proliferation, villus area and the rate of enterocyte migration. Fasting at later times resulted in smaller effects, although the jejunum appeared to be the most sensitive of the intestinal segments. Growth was correlated with the number of cells in the crypts, the number of cells along the villus and the segment surface area. The common practice whereby feed is first available to chicks more than 48 h post-hatch may depress subsequent development.

1. Post-natch mucosal development was examined in the chick small intestinal epithelium using immunostaining with proliferating cell nuclear antigen (PCNA) and 5-bromo-2-deoxyuridine (BrdU). 2. On the day of hatching jejunal crypts were small and a single crypt per villus was observed. However, during the 108 h post-hatch crypts developed rapidly branching and increasing in size, cell numbers and cell size. 3. Almost all epithelial cells in the small intestine of the hatching chick were proliferating, as indicated by PCNA and BrdU, while more than 80% of proliferating cells were localised in the crypts after 108 h post hatch. 4. Estimate of villus cell transit time using BrdU was only possible from 48 h post-hatch when villus transit time was 72 h in the jejunum, whereas at 336 h transit time was 96 h. 5. In the 108 h post hatch a rapid transition occurs from total jejunal epithelial cell proliferation and immature crypts to a defined proliferative zone in the crypts, with constant division and migration.