Scientists tested three theories as to why gene order within operons doesn't appear to be random when it comes to the order of enzymes needed in metabolic pathways. Studying E. coli and "employing deterministic and stochastic models of enzyme kinetics," the Hungarian researchers found that the theory of stochastic stalling -- if an operon is not often expressed, then all the proteins for this part of metabolism can be lost -- is supported. "Rebooting such metabolism is fastest if the operon is colinear. This model predicts, correctly, that colinearity should be more frequent in operons that are expressed at a low level," they write, suggesting that evolution of gene order can be influenced by changes in protein levels. Their work was published in PLoS Biology this week.
In PLoS Computational Biology, UC Berkeley's Lior Pachter and Robert Bradley have published a new alignment tool, Fast Statistical Alignment program. It can align protein, RNA, and DNA sequences and "improves on the accuracy of existing approaches on benchmarks of protein and RNA structural alignments and simulated mammalian and fly genomic alignments," they write in the author summary. FSA can be found here, and the source code is here.
John Postlethwait is senior author on a paper appearing in PLoS Genetics this week studying how gene loss affects the remaining genes. In a case study comparing the expression of the human retinaldehyde dehydrogenase Aldh1a gene family to the teleosts’, they found that "gene loss is indeed associated with the evolution of functional change in surviving gene family members," they say.
In PLoS One, University of Michigan scientists have created a microfluidic device for studying metastatic breast cancer cells. Their "microfluidic vasculature system" models how circulating breast cancer cells interact with the inside of blood vessels at possible sites of metastasis; as a test, they introduce CXCL12, a chemokine strongly implicated in metastasis. They found that CXCL12 acts through receptor CXCR4 on endothelium to promote adhesion of circulating breast cancer cells, independent of CXCL12 receptors CXCR4 or CXCR7 on tumor cells, they say, suggesting that "targeting CXCL12-CXCR4 signaling in endothelium may limit metastases in breast and other cancers."