Biocontrol of Postharvest Rhizopus Decay of Peaches with Pichia caribbica

A new yeast antagonist, Pichia caribbica, isolated in our laboratory from the soil collected from unsprayed orchards, was evaluated for its biocontrol capability against Rhizopus stolonifer on peaches and the possible mechanisms involved. The decay incidence and lesion diameter of Rhizopus decay of peaches treated by P. caribbica were significantly reduced compared with the control fruits, and the higher the concentration of P. caribbica, the better the efficacy of the biocontrol. Rapid colonization of the yeast in peach wounds stored at 25 °C was observed. In peaches, the activities of peroxidase (POD), catalase (CAT), and phenylalanine ammonia-lyase (PAL) were significantly induced by P. caribbica treatment compared to those of the control fruits. All these results indicated that P. caribbica has a great potential for the development of commercial formulations to control postharvest Rhizopus decay of peaches. Its modes of action were based on competition for space and nutrients with pathogens, inducement of activities of defense-related enzymes such as POD, CAT, and PAL of peaches.     

The first Praesiricidae (Hymenoptera) from Northeast China

A new subfamily Rudisiricinae Gao, Rasnitsyn, Ren & Shih, n. subfam. and a new genus Rudisiricius Gao, Rasnitsyn, Ren & Shih, n. gen. with three new species R. belli Gao, Rasnitsyn, Ren & Shih n. sp., R. crassinodus Gao, Rasnitsyn, Ren & Shih, n. sp., and R. celsus Gao, Rasnitsyn, Ren & Shih, n. sp. are described and illustrated from the family Praesiricidae. The type specimens were collected from the Late Jurassic to Early Cretaceous Yixian Formation, northeastern China. The new subfamily also includes Aulidontes Rasnitsyn from the Upper Jurassic of Karatau in Kazakhstan. This is the first record of Praesiricidae in China. These well-preserved nearly-complete new fossils reported here provide additional material and structure characters about this family, which helps filling some gap in the evolution of Lower Hymenoptera.     

Acacetin antagonized lipotoxicity in pancreatic β-cells via ameliorating oxidative stress and endoplasmic reticulum stress

Molecular Biology Reports - During the pathogenesis and progression of diabetes, lipotoxicity is a major threat to the function and survival of pancreatic β-cells. To battle against the...     

Metabolic Labeling of Leucine Rich Repeat Kinases 1 and 2 with Radioactive Phosphate

Leucine rich repeat kinases 1 and 2 (LRRK1 and LRRK2) are paralogs which share a similar domain organization, including a serine-threonine kinase domain, a Ras of complex proteins domain (ROC), a C-terminal of ROC domain (COR), and leucine-rich and ankyrin-like repeats at the N-terminus. The precise cellular roles of LRRK1 and LRRK2 have yet to be elucidated, however LRRK1 has been implicated in tyrosine kinase receptor signaling^1,2, while LRRK2 is implicated in the pathogenesis of Parkinson''s disease^3,4. In this report, we present a protocol to label the LRRK1 and LRRK2 proteins in cells with ³²P orthophosphate, thereby providing a means to measure the overall phosphorylation levels of these 2 proteins in cells. In brief, affinity tagged LRRK proteins are expressed in HEK293T cells which are exposed to medium containing ³²P-orthophosphate. The ³²P-orthophosphate is assimilated by the cells after only a few hours of incubation and all molecules in the cell containing phosphates are thereby radioactively labeled. Via the affinity tag (3xflag) the LRRK proteins are isolated from other cellular components by immunoprecipitation. Immunoprecipitates are then separated via SDS-PAGE, blotted to PVDF membranes and analysis of the incorporated phosphates is performed by autoradiography (³²P signal) and western detection (protein signal) of the proteins on the blots. The protocol can readily be adapted to monitor phosphorylation of any other protein that can be expressed in cells and isolated by immunoprecipitation.     

Characteristics and function of a low-molecular-weight compound with reductive activity from Phanerochaete chrysosporium in lignin biodegradation

A novel reductive compound with molecular weight of about 1000 Da, named Pc reducer, was purified from the liquid culture of a white-rot basidiomycete Phanerochaete chrysosporium. It was likely to have an alkene-ester structure according to Fourier-transform infrared spectroscopy (FT-IR) and nuclear magnetic resonance (NMR) spectra. Pc reducer reduced the hydroxyl radical HO and the stable nitroxide radical under certain conditions. It inhibited the repolymerization of the products from the oxidation of phenolic lignin-model compounds by reducing certain intermediate radicals. The activity of manganese peroxidases was promoted by Pc reducer at certain concentrations. Pc reducer could also weaken the repolymerization of fragments from the oxidation of Na-lignosulfonate by lignin peroxidases and manganese peroxidases. It has potential ability to improve the ligninolytic efficiency of peroxidases in P. chrysosporium.     

Identification of quantitative trait loci for shank length and growth at different development stages in chicken

Shank length affects chicken leg health and longer shanks are a source of leg problems in heavy-bodied chickens. Identification of quantitative trait loci (QTL) affecting shank length traits may be of value to genetic improvement of these traits in chickens. A genome scan was conducted on 238 F₂ chickens from a reciprocal cross between the Silky Fowl and the White Plymouth Rock breeds using 125 microsatellite markers to detect static and developmental QTL affecting weekly shank length and growth (from 1 to 12 weeks) in chickens. Static QTL affected shank length from birth to time t , while developmental QTL affected shank growth from time t− 1 to time t . Seven static QTL on six chromosomes (GGA2, GGA3, GGA4, GGA7, GGA9 and GGA23) were detected at ages of 2, 3, 4, 5, 6, 7, 9 and 12 weeks, and six developmental QTL on five chromosomes (GGA1, GGA2, GGA4, GGA5 and GGA23) were detected for five shank growth periods, weeks 2–3, 4–5, 5–6, 10–11 and 11–12. A static QTL and a developmental QTL ( SQSL1 and DQSL2 ) were identified at GGA2 (between ADL0190 and ADL0152 ). SQSL1 explained 2.87–5.30% of the phenotypic variation in shank length from 3 to 7 weeks. DQSL2 explained 2.70% of the phenotypic variance of shank growth between 2 and 3 weeks. Two static and two developmental QTL were involved chromosome 4 and chromosome 23. Two chromosomes (GGA7 and GGA9) had static QTL but no developmental QTL and another two chromosomes (GGA1 and GGA5) had developmental QTL but no static QTL. The results of this study show that shank length and shank growth at different developmental stages involve different QTL.     

Dynamic reprogramming of histone acetylation and methylation in the first cell cycle of cloned mouse embryos

Epigenetic reprogramming is thought to play an important role in the development of cloned embryos reconstructed by somatic cell nuclear transfer (SCNT). In the present study, dynamic reprogramming of histone acetylation and methylation modifications was investigated in the first cell cycle of cloned embryos. Our results demonstrated that part of somatic inherited lysine acetylation on core histones (H3K9, H3K14, H4K16) could be quickly deacetylated following SCNT, and reacetylation occurred following activation treatment. However, acetylation marks of the other lysine residues on core histones (H4K8, H4K12) persisted in the genome of cloned embryos with only mild deacetylation occurring in the process of SCNT and activation treatment. The somatic cloned embryos established histone acetylation modifications resembling those in normal embryos produced by intracytoplasmic sperm injection through these two different programs. Moreover, treatment of cloned embryos with a histone deacetylase inhibitor, Trichostatin A (TSA), improved the histone acetylation in a manner similar to that in normal embryos, and the improved histone acetylation in cloned embryos treated with TSA might contribute to improved development of TSA-treated clones. In contrast to the asymmetric histone H3K9 tri- and dimethylation present in the parental genomes of fertilized embryos, the tri- and dimethylations of H3K9 were gradually demethylated in the cloned embryos, and this histone H3K9 demethylation may be crucial for gene activation of cloned embryos. Together, our results indicate that dynamic reprogramming of histone acetylation and methylation modifications in cloned embryos is developmentally regulated.