Efficacy of plant extracts against stored-products fungi

The fungistatic activity of six aqueous extracts of plants were tested against Aspergillus candidus, Aspergillus niger, Penicillium sp. and Fusarium culmorum. The plants were, chamomile (Anthemis nobilis L.), cinnamon (Cinnamomum verum J. Presl.), French lavender (Lavandula stoechas L.), garlic (Allium sativum L.), malva (Malva sylvestris L.) and peppermint (Mentha piperita L.). The more concentrated extracts of chamomile and malva inhibited totally the growth of the tested fungi with malva the most effective one.     

Site-Specific Phosphorylation of the DNA Damage Response Mediator Rad9 by Cyclin-Dependent Kinases Regulates Activation of Checkpoint Kinase 1

The mediators of the DNA damage response (DDR) are highly phosphorylated by kinases that control cell proliferation, but little is known about the role of this regulation. Here we show that cell cycle phosphorylation of the prototypical DDR mediator Saccharomyces cerevisiae Rad9 depends on cyclin-dependent kinase (CDK) complexes. We find that a specific G2/M form of Cdc28 can phosphorylate in vitro the N-terminal region of Rad9 on nine consensus CDK phosphorylation sites. We show that the integrity of CDK consensus sites and the activity of Cdc28 are required for both the activation of the Chk1 checkpoint kinase and its interaction with Rad9. We have identified T125 and T143 as important residues in Rad9 for this Rad9/Chk1 interaction. Phosphorylation of T143 is the most important feature promoting Rad9/Chk1 interaction, while the much more abundant phosphorylation of the neighbouring T125 residue impedes the Rad9/Chk1 interaction. We suggest a novel model for Chk1 activation where Cdc28 regulates the constitutive interaction of Rad9 and Chk1. The Rad9/Chk1 complex is then recruited at sites of DNA damage where activation of Chk1 requires additional DDR–specific protein kinases.     

Mutations in PNKP Cause Recessive Ataxia with Oculomotor Apraxia Type 4

Hereditary autosomal-recessive cerebellar ataxias are a genetically and clinically heterogeneous group of disorders. We used homozygosity mapping and exome sequencing to study a cohort of nine Portuguese families who were identified during a nationwide, population-based, systematic survey as displaying a consistent phenotype of recessive ataxia with oculomotor apraxia (AOA). The integration of data from these analyses led to the identification of the same homozygous PNKP (polynucleotide kinase 3′-phosphatase) mutation, c.1123G>T (p.Gly375Trp), in three of the studied families. When analyzing this particular gene in the exome sequencing data from the remaining cohort, we identified homozygous or compound-heterozygous mutations in five other families. PNKP is a dual-function enzyme with a key role in different pathways of DNA-damage repair. Mutations in this gene have previously been associated with an autosomal-recessive syndrome characterized by microcephaly; early-onset, intractable seizures; and developmental delay (MCSZ). The finding of PNKP mutations associated with recessive AOA extends the phenotype associated with this gene and identifies a fourth locus that causes AOA. These data confirm that MCSZ and some forms of ataxia share etiological features, most likely reflecting the role of PNKP in DNA-repair mechanisms.     

Macroinvertebrate community traits and nitrate removal in stream sediments

相似文献   

Lost in the hybridisation vortex: high-elevation <Emphasis Type="Italic">Senecio hercynicus</Emphasis> (Compositae,Senecioneae) is genetically swamped by its congener <Emphasis Type="Italic">S. ovatus</Emphasis> in the Bavarian Forest National Park (SE Germany)

Hybridisation is an important evolutionary process. The investigation of hybridisation along elevational gradients, with their steep abiotic and biotic clines, provides insight into the adaptation and maintenance of species in adjacent habitats. The rare Senecio hercynicus and its spreading congener S. ovatus are vertically vicariant species that show hybridisation in their range overlaps. In the present study, we used AFLP fingerprinting of 689 individuals from 38 populations to analyse population structure and introgression patterns along four elevational transects (650–1350 m) in the Bavarian Forest National Park, Gemany. Subsequently, we searched for loci putatively under divergent selection that may maintain ‘pure’ species despite hybrid formation by identifying taxon-specific alleles. A maximum-likelihood based hybrid index shows that the overall genetic differentiation among all populations was very low with a vanishingly small number of pure parental individuals. Almost 75% of the investigated individuals were classified as backcrosses towards S. ovatus. The highest S. hercynicus ancestry was found in the uppermost populations of two transects. Further, we found seven taxon-specific alleles being under divergent selection that correlated with climatic variables and deviating from neutral introgression. According to our results, hybridisation of S. ovatus and S. hercynicus has reached an advanced state of genetic swamping and there seems to be no driving force that is strong enough to keep both species as different lineages. Rather, S. ovatus appears to benefit through putatively adaptive introgression.     

Cytoplasmic thioredoxin reductase is essential for embryogenesis but dispensable for cardiac development

Two distinct thioredoxin/thioredoxin reductase systems are present in the cytosol and the mitochondria of mammalian cells. Thioredoxins (Txn), the main substrates of thioredoxin reductases (Txnrd), are involved in numerous physiological processes, including cell-cell communication, redox metabolism, proliferation, and apoptosis. To investigate the individual contribution of mitochondrial (Txnrd2) and cytoplasmic (Txnrd1) thioredoxin reductases in vivo, we generated a mouse strain with a conditionally targeted deletion of Txnrd1. We show here that the ubiquitous Cre-mediated inactivation of Txnrd1 leads to early embryonic lethality. Homozygous mutant embryos display severe growth retardation and fail to turn. In accordance with the observed growth impairment in vivo, Txnrd1-deficient embryonic fibroblasts do not proliferate in vitro. In contrast, ex vivo-cultured embryonic Txnrd1-deficient cardiomyocytes are not affected, and mice with a heart-specific inactivation of Txnrd1 develop normally and appear healthy. Our results indicate that Txnrd1 plays an essential role during embryogenesis in most developing tissues except the heart.