The New York Times profiles GlaxoSmithKline's Andrew Witty, particularly focusing on his efforts to help the poor. Witty has promised to limit the price of GSK drugs in poor countries to no more than 25 percent of what they charge in wealthy nations and to donate one-fifth of the profits from poor countries to build up their healthcare systems. Witty, of course, has his detractors. Daniel Berman, who began the Doctors Without Borders' Access Campaign says that moving vaccine technology to middle-income countries was "still a lot of smoke and mirrors" and that GSK's malaria-focused lab in Spain "still doesn't have a big enough budget to make a difference." Witty has won over others, including Oxfam's Sophia Tickell. "I'm in charge of an organization that can actually make a difference for people in the third world, and I am not going to be the person who, after X years, sits back and says, 'Oh, I wish I'd done more,'" Witty says.

This week in the PNAS Early Edition, researchers show a relationship between RNA polymerases II and III by using ChIP-Seq studies to map their in vivo binding sites throughout the human genome. In the investigation of two cell lines, GM12878 and K562, Pol II was found to bind near many known Pol III genes, as well as a number of previously unidentified Pol III targets. The team also found that transcription factors normally associated with Pol II transcription were also closely connected with Pol-III-transcribed genes. Their results refute the previous expectation that RNA polymerases operate independently from one another, showing that Pol II and Pol III can work together to globally coordinate gene expression.

Research of out of Iowa State University demonstrates that AtIWS1, a protein implicated with the post-recruitment and transcription elongation processes of RNA polymerase II in Arabadopsis thaliana, is required for brassinosteroid-induced gene expression. The researchers found that loss-of-function mutations in AtIWS1 resulted in overall dwarfism, hypersensitivity to a transcription elongation inhibitor, reduced BR response, and, therefore, a genome-wide decrease in BR-induced expression in the model plant. The team writes that their study establishes an important role for AtIWS1 in plant steroid-induced gene expression and also suggests the possibility that the protein can be used as a target for pathway-specific activators in Arabidopsis.

In this week's advance online publication of PNAS, California Institute of Technology researchers discuss connections within the neural crest gene regulatory network, specifically the function of Sox10 as one of the earliest neural crest-specifying genes. The team found that Sox10 drives delamination and directly regulates several downstream effectors and differentiation gene batteries. In performing ChIP, DNA pull-down, and gel-shift assay experiments, the team also demonstrates Sox10E2 - the earliest acting neural crest cis-regulatory element-binding to its enhancer in vivo. This cis-regulatory analysis helped the researchers to establish the direct link of upstream effectors to a key neural crest specifier.

Also in PNAS this week, Markus Rinschen and his international colleagues describe their use of mass spectrometry-based quantitative phosphoproteomics to identify signaling pathways involved in the short-term V2-receptor-mediated response in murine renal collecting duct cells. Using the mouse model, Rinschen's team created two treatment groups: one received 0.1 nM dDAVP, the other merely the treatment vehicle. In the quantification of 2884 phosphopeptides, the researchers establish the roles of multiple V2-receptor-dependent signaling pathways in the vasopression signaling network of collecting duct cells.

Researchers are hoping to capture some of the diversity seen in Latin Americans through the new Slim Initiative for Genomic Health between the Broad Institute and Mexico City's Carlos Slim Health Institute, says MIT's Technology Review. That project is still in the planning stages — though it will include gene sequencing and microarray-based studies — but INMEGEN published a Mexican version of the HapMap last year. "We can clearly see different components in the admixture pattern in the Mexican population," says Gerardo Jimenez-Sanchez, former director of INMEGEN. "We can also observe that the Mexican population is a range of admixture from those individuals who are very European to those who are very indigenous." Jimenez-Sanchez adds that "if personalized medicine is going to become a global phenomenon, then scientists need to understand the genomes of all the world's population."

In this week's issue of PLoS Genetics, researchers at the University of Georgia report their identification of the DNA-binding domain of a centromere binding protein, CENPC, in maize. They demonstrate that CENPC requires a single-stranded RNA to effectively bind DNA in vitro, and, when absent, the accuracy of CENPC targeting to centromeres is reduced. The authors report that their results support the notion that RNA binding ensures that centromeres are stably inherited, a critical function of the epigenetic determination process.

Also in PLoS Genetics, Neil Morgan and colleagues identify mutations of the gene SLC29A3 as the molecular basis for a familial form of syndromic histiocytosis, confirming a direct link between Faisalabad histiocytosis and Rosai-Dorfman disease, as well as other associated phenotypes. Mutations in SLC29A3, characteristic of these disorders, cause the generation of excessive histiocytes which phagocytose other cells and process antigens. The authors surmise that their discoveries will shed light on the pathophysiology of histiocytic disorders, which have been recognized for nearly a century, but have afforded no disease-specific treatments.

Researchers report a universal trend of reduced mRNA stability near the translation-initiation site in both prokaryotes and eukaryotes in PLoS Computational Biology. Using computational methods to predict the thermodynamic stability of mRNA downstream from the start codon, and information from the complete genomes of 340 species, the team found that, in nearly all species, mRNA stability is reduced near the start codon, and that the reduction of stability correlates with the increasing genomic GC content. While the team did not find a genome-wide trend of reduced mRNA stability near the start codon in birds and mammals, they did find such a reduction in the most GC-rich genes.

Meanwhile, in PLoS One, an international team describes VAV2 and VAV3 as candidate disease genes for spontaneous glaucoma in both mice and humans. VAV2/VAV3-deficient mice show early onset of iridocorneal angle alterations and elevated intraocular pressure with the subsequent loss of retinal gangilion cells and optical nerve head cupping, characteristic of glaucoma, which is the leading cause of blindness in humans. The researchers posit that VAV2/VAV3-deficient mice could serve as a useful model to study the pathogenesis of glaucoma in humans.

To close its $150 million budget gap, Yale University will be cutting staff, freezing salaries, and limiting the number of graduate students, reports the New York Times. A memo from Yale’s president and its provost, Richard Levin and Peter Salovey, said these steps were needed because the school's endowment dropped from $22.9 billion in June 2008 to $16.3 billion in June 2009. The Times adds that the memo did not say how many positions would be cut, though the reduction in gradates students will be between 10 and 15 percent. Also, Yale will be turning its heat down, setting thermostats to 68 degrees.