Microfluidic affinity and ChIP-seq analyses converge on a conserved FOXP2-binding motif in chimp and human, which enables the detection of evolutionarily novel targetsNucleic Acids Research, 2013
ACBD3 Interaction with TBC1 Domain 22 Protein Is Differentially Affected by Enteroviral and Kobuviral 3A Protein BindingmBio, 2013
Bartonella quintana Deploys Host and Vector Temperature-Specific TranscriptomesPLos One 2013
Identification and manipulation of the molecular determinants influencing poliovirus recombination.PLoS Pathogen, 2013
Splenic Red Pulp Macrophages Produce Type I Interferons as Early Sentinels of Malaria Infection but Are Dispensable for ControlPLoS One 2012
Programmable microfluidic synthesis of spectrally encoded microspheresLab on a Chip 2012
Basic leucine zipper transcription factor Hac1 binds DNA in two distinct modes as revealed by microfluidic analysesPNAS 2012
We are pleased to release PRICE (Paired-Read Iterative Contig Extension), a de novo genome assembler implemented in C++. Its name describes the strategy that it implements for genome assembly: PRICE uses paired-read information to iteratively increase the size of pre-assembled contigs. It was designed to address the challenge of assembling viral genomes that constituted a small minority of the reads within ultra-deep, short-read, metagenomic, shotgun datasets. PRICE has already enabled the discovery of several novel virus genomes from such complex datasets.
The early online edition of the PRICE paper, published in G3, is here.Download PRICE
For many years, a mysterious disease in boa constrictors and pythons called Inclusion Body Disease (IBD) has been the scourge of aquariums, breeders, and pet snake owners. The disease is ultimately fatal, and until now, its cause was unknown. Using the latest methods in ultra deep sequencing and de novo sequence assembly, the DeRisi lab, in collaboration with the California Academy of Science and local veterinarians, has identified a novel snake arenavirus that is closely linked to the disease. The paper describing this discovery is published in ASM's new open-access journal mBio, to be released August 14th.
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Malaria caused by Plasmodium spp parasites is a profound human health problem that has shaped our evolutionary past and continues to influence modern day with a disease burden that disproportionately affects the world's poorest and youngest. A plastid organelle, the apicoplast, has been hailed as Plasmodium's Achilles' heel? because it contains bacteria-derived pathways that have no counterpart in the human host and therefore may be ideal drug targets. In this study, we use a simple chemical method to generate parasites that have lost their apicoplast, normally a deadly event, but which survive rescued by the addition of an essential metabolite to the culture. This chemical rescue demonstrates that the apicoplast serves only a single essential function, namely isoprenoid precursor biosynthesis during blood-stage growth, validating this metabolic function as a viable drug target. Moreover, the apicoplast-minus Plasmodium strains generated in this study will be a powerful tool for identifying apicoplast-targeted drugs and as a potential vaccine strain with significant advantages over current vaccine technologies.Read the Full Press Release Here