Genome Sequences of Two Strains from Nectarines Associated with Listeriosis in 2014.

is an important foodborne pathogen. Here, we present the annotated whole genome of strains F14M01297-C2 and F14M01297-C4, isolated from nectarines distributed by a packing facility in California during an investigation of listeriosis associated with stone fruit in 2014.

Moloney leukemia virus type 10 inhibits reverse transcription and retrotransposition of intracisternal a particles.

Moloney leukemia virus type 10 protein (MOV10) is an RNA helicase that is induced by type I interferon. It inhibits HIV replication at several steps of its replicative cycle. Of interest, MOV10 is a component of mRNA processing (P) bodies, which inhibit retrotransposition (RTP) of intracisternal A particles (IAP).

P bodies inhibit retrotransposition of endogenous intracisternal a particles.

mRNA-processing bodies (P bodies) are cytoplasmic foci that contain translationally repressed mRNA. Since they are important for the retrotransposition of Ty elements and brome mosaic virus in yeast cells, we assessed the role of P bodies in the movement of endogenous intracisternal A particles (IAPs) in mammalian cells. In contrast to the case for these other systems, their disruption via knockdown of RCK or eukaryotic initiation factor E transporter (eIF4E-T) increased IAP retrotransposition as well as levels of IAP transcripts, Gag proteins, and reverse transcription products.

Frataxin deficiency induces Schwann cell inflammation and death.

Mutations in the frataxin gene cause dorsal root ganglion demyelination and neurodegeneration, which leads to Friedreich's ataxia. However the consequences of frataxin depletion have not been measured in dorsal root ganglia or Schwann cells. We knocked down frataxin in several neural cell lines, including two dorsal root ganglia neural lines, 2 neuronal lines, a human oligodendroglial line (HOG) and multiple Schwann cell lines and measured cell death and proliferation.

Cell functions impaired by frataxin deficiency are restored by drug-mediated iron relocation.

Various human disorders are associated with misdistribution of iron within or across cells. Friedreich ataxia (FRDA), a deficiency in the mitochondrial iron-chaperone frataxin, results in defective use of iron and its misdistribution between mitochondria and cytosol. We assessed the possibility of functionally correcting the cellular properties affected by frataxin deficiency with a siderophore capable of relocating iron and facilitating its metabolic use.

Frataxin knockdown causes loss of cytoplasmic iron-sulfur cluster functions, redox alterations and induction of heme transcripts.

Frataxin protein deficiency causes the neurodegenerative disease Friedreich ataxia. We used inducible siRNA to order the consequences of frataxin deficiency that we and others have previously observed. The earliest consequence of frataxin deficiency was a defect in cytoplasmic iron-sulfur proteins.

[Study of microsatellite polymorphisms between the Han nationality and French population by fluorescence-based genotype].

Objective: To facilitate the application of the large scale genome scan and individual identification by investigating the differences of microsatellite polymorphisms of the genethon human genetic linkage map between the Han nationality and French population.

Methods: Six to seventeen pairs of primers were added in one single tube with 5 microliters reaction volume and several microsatellite markers were amplified simultaneously. The products were electrophoresited on the 377XL DNA sequencer.

[Molecular cloning of the human CX 58 gene].

Objective: To clone a novel human connexin gene and find out the relationship between this gene and hereditary deafness.

Methods: Through the basic local alignment search tool (BLAST) analysis against the database of expressed sequence tags (dbEST) of National Center for Biotechnology Information (NCBI) using the coding sequence of mouse Cx 57 gene, 9 novel ESTs were obtained and a contig was assembled. Nested polymerase chain reaction (PCR) and rapid amplification of cDNA ends (RACE) were performed using primers designed on the contig.