A ten-week feeding trial was conducted to evaluate the effect of replacing fishmeal with two differently processed cottonseed meals (CSM), namely XC and SC, separately in turbot (5.28 ± 0.02 g). Nine isonitrogenous and isoenergetic diets were formulated without fishmeal replacement (FM), 150 g/kg (XC15, SC15), 250 g/kg (XC25, SC25), 350 g/kg (XC35, SC35) and 450 g/kg (XC45, SC45) of fishmeal replaced by CSM.Fishmeal was successfully replaced by XC in turbot diets without growth reduction at 350 g/kg, but not by SC even at 150 g/kg. The apparent digestibility coefficients of SC-included diets were significantly lower than XC-included diets at same replacement level. The activities of aspartate aminotransferase and superoxide dismutase were significantly affected in XC45 and SC45 group. The XC45 and SC-included diets caused shortened distal intestine villi height and structural damage of liver compared with FM diet. This study indicated that different processing methods could affect the nutritional value of CSM and effect as a protein source for turbot. CSM with high quality could be an important alternative dietary protein source for juvenile turbot. K E Y W O R D Sapparent digestibility coefficients, cottonseed meal, growth performance, haematological, intestinal and liver morphology, turbot

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Our data demonstrate that TET2 works as an epigenetic regulator of Rosi-mediated insulin sensitization and transcriptional regulation in adipocytes.

Gossypol is known to be a polyphenolic compound toxic to animals. However, its molecular targets are far from fully characterized. To evaluate the physiological and molecular effects of gossypol, we chose turbot (Scophthalmus maximus L.), a carnivorous fish, as our model species. Juvenile turbots (7.83 ± 0.02 g) were fed diets containing gradient levels of gossypol at 0 (G0), 600 (G1), and 1,200 (G2) mg/kg diets for 11 wk. After the feeding trial, fish growth, body protein, and fat contents were significantly reduced in the G2 group compared with those of the G0 group (P < 0.05). Gossypol had little impact on digestive enzyme activities and intestine morphology. However, gossypol caused liver fibrosis and stimulated chemokine and proinflammatory cytokine secretions. More importantly, gossypol suppressed target of rapamycin (TOR) signaling and induced endoplasmic reticulum (ER) stress pathway in both the feeding experiment and cell cultures. Our results demonstrated that gossypol inhibited TOR signaling and elevated ER stress pathways both in vivo and in vitro, thus providing new mechanism of action of gossypol in nutritional physiology.

Vsx2 is a transcription factor essential for retinal proliferation and bipolar cell differentiation but the molecular mechanisms underlying its developmental roles are unclear. Here, we profiled VSX2 genomic occupancy during mouse retinogenesis, revealing extensive retinal genetic programs associated with VSX2 during development. VSX2 binds and transactivates its enhancer in association with the transcription factor PAX6. Mice harboring deletions in the Vsx2 regulatory landscape exhibit specific abnormalities in retinal proliferation and bipolar cell differentiation. In one of those deletions, a complete loss of bipolar cells is associated with a bias toward photoreceptor production. VSX2 occupies cis-regulatory elements nearby genes associated with photoreceptor differentiation and homeostasis in the adult mouse and human retina, including a conserved region nearby Prdm1, a factor implicated in the specification of rod photoreceptors and suppression of bipolar cell fate. VSX2 interacts with the transcription factor OTX2 and can act to suppress OTX2-dependent enhancer transactivation of Prdm1 enhancer. Taken together, our analyses indicate that Vsx2 expression can be temporally and spatially uncoupled at the enhancer level and illuminate important mechanistic insights on how VSX2 is engaged with gene regulatory networks essential for retinal proliferation and cell fate acquisition.