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In silicopredicted behavior of four synthetic gene networks. Ellis et al. engineer networks with predictable behavior using libraries of experimentally and mathematically characterized promoters (p 465). Credit: Kimberly Caesar.
Lawyer Richard Gold argues that superfluous patents stifle innovation. Industry should adopt new models, he says, in which knowledge is viewed as a club good.
As the economic downturn chokes spin-outs from academia, a spate of newly minted university-industry partnerships are springing up. Failing to address the financial conflicts in such partnerships could spell trouble for both faculty and drug companies. Jim Kling investigates.
The biotech sector must not only maintain an emphasis on ground-breaking products and focus on retaining key staff but also mobilize to ensure that US health policy continues to reward its innovations.
Synthetic gene networks can be readily redesigned using new libraries of quantitatively characterized promoters coupled with predictive mathematical modeling.
Mapping the vast quantities of short sequence fragments produced by next-generation sequencing platforms is a challenge. What programs are available and how do they work?
Judson et al. show that microRNAs specific to mouse embryonic stem cells can substitute for the reprogramming factor cMyc in the generation of induced pluripotent stem cells. The development of reprogramming methods that do not rely on transgenes may facilitate clinical translation of this technology.
Hosaka et al. show that selection of bacteria for antibiotic resistance can be used to discover new antibacterials. Some of the mutant strains they generated, which bear mutations in RNA polymerase and in a ribosomal protein, produce a previously unknown class of antibacterial called piperidamycin.
Ellis et al. describe a strategy for rationally assembling gene networks with predictable behaviors. Using mathematical models, they predict the responses of complex synthetic gene networks built from quantitatively characterized promoter libraries, and harness these networks to regulate an industrially relevant yeast phenotype.
Single-nucleotide polymorphisms in microRNA target sites can disrupt the effects of the microRNA. Kim and Bartel use sequencing to investigate this phenomenon on a large scale and find that such polymorphisms generate gene-regulatory diversity in mice.
Strategies for allele-specific knockdown of the mutant genes in triplet-repeat disorders have relied on point or deletion mutations that differ among affected individuals. Hu et al. show that antisense oligomers can selectively recognize expanded CAG repeats in mRNAs, allowing silencing of mutant but not wild-type alleles.