In order to identify the genes involved in the fatness variability, we studied the expression of several genes implicated in the hepatic lipid metabolism of broiler chickens with different fat deposition patterns during embryonic development. The mRNA expression of acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), malic enzyme (ME) and apolipoprotein B100 (apoB100) genes were determined using reverse transcriptase-polymerase chain reaction (RT-PCR). Samples of livers were collected from Arbor Acres (AA) and Sanhuang (SH) chickens on day 9, 14 and 19 of embryonic development as well as at hatching. This study showed that hepatic triglyceride (TG) level was found to increase suddenly during day 14 of embryonic development, to gradually increase thereafter, and to remain relatively constant at hatching. FAS gene expression in AA and SH broilers occurred prior to hatching and at hatching. The gene was expressed more in the former breed. ACC gene expression was observed beginning at the earlier development stage of days 9. No breed difference was observed in ME and apoB gene expression. This study indicated that the expression of lipogenic enzyme genes of the liver in broiler chickens exhibited scheduling during embryogenesis. The ACC gene started to express earlier than the FAS gene during embryonic development. This suggested that embryonic liver synthesized fatty acid, and breed difference was noticed prior to hatching.
Fusarium head blight (FHB), caused by Fusarium graminearum, is one of the most devastating wheat diseases in China. Phenamacril is a novel cyanoacrylate fungicide with a unique chemical structure and specific mode of action against Fusarium spp. In this study, the molecular, biological and physiological characteristics of laboratory-induced mutants of F. graminearum with resistance to phenamacril were investigated. Compared to the wildtype strains, the phenamacril-resistant mutants showed obvious defects in various biological and physiological characteristics, including vegetative growth, carbon source utilization, response to oxidative and osmotic stresses, sensitivity to cell wall and cell membrane integrity inhibitors, cell membrane permeability, glycerol accumulation and pathogenicity. The phenotypes of the phenamacril-resistant mutants exhibited many variations. Sequencing indicated that the three parental strains studied were identical, and the mutants TXR1, TXR2, BMR1, BMR2, SYR1 and SYR2 each had a single point mutation in the amino acid sequence encoded by the myosin-5 gene (FGSG_01410). These results provide new reference information for future investigations concerning the resistance mechanism of F. graminearum to phenamacril and could offer important relevant data for the management of FHB caused by F. graminearum.
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