In Science Signaling this week, researchers in Germany report on their loss-of-function RNAi screen which revealed Ras- and Raf-independent MEK-ERK signaling in human epithelial cells during Chlamydia trachmatis infection. Their study also identified 59 host factors that either positively or negatively influenceChlamydia replication; depletion of Ras or Raf in HeLa cells increased the pathogen's growth. "Together, these findings not only show that Chlamydia regulates components of an important host cell signaling pathway, but also provide mechanistic insights into how this is achieved," the authors write.
In Science Translational Medicine, an international research team presents evidence that mutations in fibrillin-1 cause Stiff Skin Syndrome, an autosomal dominant congenital form of scleroderma. The researchers found that mutations in the only Arg-Gly-Asp sequence-encoding domain of fibrillin-1 — wherein integrin binding is mediated — causes the condition, which involved fibrosis and hardening of the skin. "The observation of similar findings in systemic sclerosis, a more common acquired form of scleroderma, suggests broad pathogenic relevance," they write.
In an advance, online publication of Science this week, investigators in Japan and the US report that inactivation of the dcr-1 gene in Caenorhabditis elegans "compromises apoptosis and blocks apoptotic chromosome fragmentation." Their studies show that DCR-1 fragments chromosomal DNA during apoptosis — in addition to processing small RNAs — and undergoes a "protease-mediated conversion from a ribonuclease to a deoxyribonuclease."
A report in Science this week describes CKAMP44 as a brain-specific type I transmembrane protein that modulates short-term plasticity at specific excitatory synapses. Using a proteomic approach, researchers found that CKAMP44 expressed in Xenopus oocytes "reduced GluA1- and A2-mediated steady-state currents, but did not affect kainate- or N-methyl- D-aspartate receptor-mediated currents." In a mouse model, hippocampal CA1 pyramidal neurons expressed CKAMP44 at low abundance; dentate gyrus granule cells exhibited strong CKAMP 44 expression.