Field Observations on the Effect of a Mannan Oligosaccharide on Mortality and Intestinal Integrity of Sole (Solea senegalensis, Kaup) Infected by Photobacterium damselae subsp. piscicida

This study was conducted in order to investigate the effect of a mannan oligosaccharide (MOS) on the intestinal morphology of sole (Solea senegalensis, Kaup) reared under commercial conditions. The dietary inclusion rate for MOS was 0.4% and it was used either alone or in combination with a vaccination regime against bacterial diseases (Pasteurella spp. and Vibrio spp.). One week after the start of the experimental period, a natural outbreak of pasteurellosis, caused by Photobacterium damselae subsp.piscicida,occurred in all the groups of fish.A two-way ANOVA showed that only MOS supplementation reduced fish mortality by ca. 8% (P = 0.050). Additionally, light microscopy examination of the intestine revealed that MOS supplementation significantly increased the mucosal folding by 29% (P = 0.016) in the anterior intestinal region and by 33% (P = 0.002) in the posterior intestinal region. Scanning electron microscopy demonstrated that both MOS supplementation and vaccination significantly increased microvilli density on the enterocyte surfaces in the anterior intestinal regionby 13% (P = 0.028) and 30% (P = 0.001) respectively. In the posterior intestinal region neither MOS supplementation nor vaccination significantly affected the microvilli density (P = 0.005).The present study suggests that dietary MOS supplementation protects the intestinal morphology of infected sole and hinders the development of pathogenic infection, possibly by binding with Photobacterium damselae subsp. piscicida, resulting in reduced mortality of infected fish

Stem Cell Factor SALL4 Represses the Transcriptions of PTEN and SALL1 through an Epigenetic Repressor Complex

Background The embryonic stem cell (ESC) factor, SALL4, plays an essential role in both development and leukemogenesis. It is a unique gene that is involved in self-renewal in ESC and leukemic stem cell (LSC).Methodology/Principal Findings To understand the mechanism(s) of SALL4 function(s), we sought to identify SALL4-associated proteins by tandem mass spectrometry. Components of a transcription repressor Mi-2/Nucleosome Remodeling and Deacetylase (NuRD) complex were found in the SALL4-immunocomplexes with histone deacetylase (HDAC) activity in ESCs with endogenous SALL4 expression and 293T cells overexpressing SALL4. The SALL4-mediated transcriptional regulation was tested on two potential target genes: PTEN and SALL1. Both genes were confirmed as SALL4 downstream targets by chromatin-immunoprecipitation, and their expression levels, when tested by quantitative reverse transcription polymerase chain reaction (qRT-PCR), were decreased in 293T cells overexpressing SALL4. Moreover, SALL4 binding sites at the promoter regions of PTEN and SALL1 were co-occupied by NuRD components, suggesting that SALL4 represses the transcriptions of PTEN and SALL1 through its interactions with the Mi-2/NuRD complex. The in vivo repressive effect(s) of SALL4 were evaluated in SALL4 transgenic mice, where decreased expressions of PTEN and SALL1 were associated with myeloid leukemia and cystic kidneys, respectively.Conclusions/Significance In summary, we are the first to demonstrate that stem cell protein SALL4 represses its target genes, PTEN and SALL1, through the epigenetic repressor Mi-2/NuRD complex. Our novel finding provides insight into the mechanism(s) of SALL4 functions in kidney development and leukemogenesis