In a paper published online in advance in Science this week, an international team led by investigators at Canada's University of Alberta reports having "expanded the palette" of engineered fluorescent protein chimeras to include blue, red, an "improved green" as well as an "emission ratiometric indicator with an 11,000-percent ratio change." Using this series of indicators "improved single-color Ca2+ imaging in neurons and transgenic Caenorhabditis elegans," the authors write, adding that in HeLa cells, they were able to image Ca2+ in three subcellular comparments. "In conjunction with a CFP-YFP–based indicator, Ca2+ and adenosine 5′-triphosphate were simultaneously imaged," in HeLa cells, the researchers say.
Over in this week's issue, researchers at Pennsylvania State University and elsewhere describe what they call "a gene for extended phenotype" in the Lymantria dispar gypsy moth nucleopolyhedrovirus, or LdMNPV — that manipulates climbing behavior observed in moth larvae infected by the baculovirus. Infected larvae, the authors say, "climb to the top of trees to die, liquefy, and 'rain' virus on the foliage below to infect new hosts," whereas usually "L. dispar hide in bark crevices or climb down the tree ... to avoid predation from birds." The Penn State-led team pinned the viral gene responsible for this moth behavior down to the egt gene. "These results provide a genetic basis for the extended phenotype whereby a gene in one organism (the parasite) has phenotypic effects on another organism (the host)," the authors conclude.
Harvard University's Wenqin Wang et al. report their use of "super-resolution fluorescence microscopy in combination with a chromosome-conformation capture assay to study the distributions of major NAPs [nucleoid-associated proteins] in live Escherichia coli cells." The team identifies H-NS, a global transcriptional silencer, as crucial to chromosome organization.
Elsewhere in this week's Science, the University of Cambridge Edward Emery et al. show that mice in which deletion of HCN2 in nociceptors expressing NaV1.8 show "normal pain thresholds," and says that "neuropathic pain is ... initiated by HCN2-driven action potential firing in NaV1.8-expressing nociceptors."