An 8-week feeding trial was conducted to evaluate optimum dietary methionine (Met) requirement of juvenile humpback grouper (Cromileptes altivelis) and the influence of dietary methionine (Met) supplementations on growth, gut micromorphology, protein and lipid metabolism. Seven isoproteic (48.91%) and isolipidic diets (10%) were made to contain 0.70, 0.88, 1.04, 1.27 1.46, 1.61 and 1.76% of dry matter Met levels. Results showed that lower survival, weight gain (WG%), protein efficiency ratio (PER), protein productive value (PPV) but higher daily feed intake (DFI) and feed conversion ratio (FCR) were observed in the Met deficient groups (0.70 and 0.88%). Optimum dietary Met requirement for humpback grouper was found to be 1.07% through the straight-broken line analysis of WG% against Met. Fish fed Met deficient diets (0.70, 0.88%) exhibited lower mRNA levels of growth hormone (GH), growth hormone receptor (GHR), insulin-like growth factor-I (IGF-1), target of rapamycin (TOR) as well as S6 kinase 1 (S6K1) than other dietary groups. Whereas, expression of genes related to general control nonderepressible (GCN2) kinase i.e., GCN2 and C/EBPβ enhancer-binding protein β was upregulated in fish fed low Met diets (P < 0.05). The mRNA expression of hepatic fatty acid synthase (FAS) and sterol regulatory element-binding protein-1 (SREBP-1) were higher in fish fed 0.70 and 0.88% dietary Met group and the lipolytic genes, hepatic peroxisome proliferator-activated receptor α (PPARα) and carnitine palmitoyl transferase-1 (CPT-1) showed an opposite variation tendency as FAS or SREBP1. Generally, the optimum Met requirement for humpback grouper was predicted to be 1.07% of dry matter.
A novel Gram-staining positive, aerobic, rod-shaped, non-motile and yellow-pigmented actinobacterium, designated strain WY83T, was isolated from a marine sediment of Indian Ocean. Strain WY83T grew optimally at 30–35 °C, pH 7–8 and with 0–3% (w/v) NaCl. The predominant menaquinones were MK-10, MK-11 and MK-12, and the major fatty acids were C19:1 ω9c/C19:1 ω11c, anteiso-C15:0, C17:0 3OH, and iso-C16:0. The polar lipids consisted of diphosphatidylglycerol, phosphatidylglycerol and one unidentified glycolipid. The cell-wall peptidoglycan contained lysine as a diamino acid. The DNA G?+?C content was 72.3 mol%. Phylogenetic analysis based on 16S rRNA gene sequences and ninety-two bacterial core genes indicated that strain WY83T formed an evolutionary lineage with Chryseoglobus frigidaquae JCM 14730T, Chryseoglobus indicus CTD02-10-2T, Yonghaparkia alkaliphila JCM 15138T, Microcella alkaliphila DSM 18851T and Microcella putealis DSM 19627T within the radiation enclosing members of the family Microbacteriaceae. All pairwise percentage of conserved proteins between strain WY83T and the closely related phylogenetic neighbors were greater than 65%. The average nucleotide identity and in silico DNA–DNA hybridization values were both below the thresholds used for the delineation of a new species. On the basis of the evidence presented, strains WY83T, Y. alkaliphila JCM 15138T, C. frigidaquae JCM 14730T, M. alkaliphila DSM 18851T and M. putealis DSM 19627T should belong to different species of the same genus. Strain WY83T represents a novel species of the genus Microcella, for which the name Microcella flavibacter sp. nov. is proposed. The type strain is WY83T (=?KCTC 39637T?=?MCCC 1A07099T). Furthermore, Chryseoglobus frigidaquae, Chryseoglobus indicus, and Yonghaparkia alkaliphila were reclassified as Microcella frigidaquae comb. nov., Microcella indica nom. nov., and Microcella alkalica nom. nov., respectively.
Recent reports showed that haematological and neurological expressed 1-like (HN1L) gene participated in tumorigenesis and tumour invasion. However, the expression and role of HN1L in breast cancer remain to be investigated. Here, bioinformatics, western blot and immunohistochemistry were used to detect the expression of HN1L in breast cancer. Wound healing, transwell assay, immunofluorescence assay and mass spectrum were used to explore the role and mechanism of HN1L on the migration and invasion of breast cancer, which was confirmed in vivo using a nude mice model. Results showed that HN1L was significantly over-expressed in breast cancer tissues, which was positively correlated with M metastasis of breast cancer patients. Silencing HN1L significantly inhibited the invasion and metastasis of breast cancer cells in vitro and lung metastasis in nude mice metastasis model of breast cancer. Mechanistically, HN1L interacted with HSPA9 and affected the expression of HMGB1, playing a key role in promoting the invasion and metastasis of breast cancer cell. These results suggested that HN1L was an appealing drug target for breast cancer. 相似文献
The use of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) is limited in drug discovery and cardiac disease mechanism studies due to cell immaturity. Micro-scaled grooves can promote the maturation of cardiomyocytes by aligning them in order, but the mechanism of cardiomyocytes alignment has not been studied. From the level of calcium activity, gene expression and cell morphology, we verified that the W20H5 grooves can effectively promote the maturation of cardiomyocytes. The transient receptor potential channels (TRP channels) also play an important role in the maturation and development of cardiomyocytes. These findings support the engineered hPSC-CMs as a powerful model to study cardiac disease mechanism and partly mimic the myocardial morphological development. The important role of the TRP channels in the maturation and development of myocardium is first revealed. 相似文献
Genetic variation plays a fundamental role in pathogen''s adaptation to environmental stresses. Pathogens with low genetic variation tend to survive and proliferate more poorly due to their lack of genotypic/phenotypic polymorphisms in responding to fluctuating environments. Evolutionary theory hypothesizes that the adaptive disadvantage of genes with low genomic variation can be compensated for structural diversity of proteins through post‐translation modification (PTM) but this theory is rarely tested experimentally and its implication to sustainable disease management is hardly discussed. In this study, we analyzed nucleotide characteristics of eukaryotic translation elongation factor‐1α (eEF‐lα) gene from 165 Phytophthora infestans isolates and the physical and chemical properties of its derived proteins. We found a low sequence variation of eEF‐lα protein, possibly attributable to purifying selection and a lack of intra‐genic recombination rather than reduced mutation. In the only two isoforms detected by the study, the major one accounted for >95% of the pathogen collection and displayed a significantly higher fitness than the minor one. High lysine representation enhances the opportunity of the eEF‐1α protein to be methylated and the absence of disulfide bonds is consistent with the structural prediction showing that many disordered regions are existed in the protein. Methylation, structural disordering, and possibly other PTMs ensure the ability of the protein to modify its functions during biological, cellular and biochemical processes, and compensate for its adaptive disadvantage caused by sequence conservation. Our results indicate that PTMs may function synergistically with nucleotide codes to regulate the adaptive landscape of eEF‐1α, possibly as well as other housekeeping genes, in P. infestans. Compensatory evolution between pre‐ and post‐translational phase in eEF‐1α could enable pathogens quickly adapting to disease management strategies while efficiently maintaining critical roles of the protein playing in biological, cellular, and biochemical activities. Implications of these results to sustainable plant disease management are discussed. 相似文献
96序列相似的家庭成员A和B(family with sequence similarity 96 member A and B,FAM96A和FAM96B)是属于MIP18(MMS19-interacting protein of 18 kD)家族的2个高度保守的同源蛋白,MIP18是与有丝分裂纺锤体相关的MMDX(MMS19-MIP18-XPD)复合体的亚基。研究表明,FAM96A和FAM96B在人胃肠道间质瘤、结肠癌、肝癌、胃癌和乳腺癌等多种肿瘤组织中的表达显著降低,提示其可能是作为潜在的抑癌基因参与肿瘤的发生发展,但目前关于FAM96A和FAM96B在肿瘤发生发展过程中的作用机理并不十分清楚。此外,研究发现FAM96A和FAM96B可通过与其他不同的蛋白质相互作用在体内发挥多种不同的功能。因此,就目前对于FAM96A和FAM96B结构和功能的研究所取得的进展进行了回顾与总结,并对其在肿瘤发生发展中的分子机制和相互作用蛋白鉴定的研究前景进行了展望,以期为临床上将FAM96A和FAM96B作为新的肿瘤诊断标志物和治疗靶点奠定基础,并为揭示二者在体内更多的新功能提供依据。 相似文献