Harvard University's planned academic science center in Allston, Mass., is on "pause," says Science. Only the foundation will be finished. The planned 50,000-square-meter facility was to be home to cutting-edge research in biology, engineering, and medicine. Harvard has lost 30 percent of its endowment and expects to see fewer donations.
Science has a retrospective looking at the work of Frederic Richards, who died in January at age 83. In the 1950s, Richards showed that the product of adding the protease subtilisin to RNase A was RNase S, which was still active. He later reported that two inactive fragments of RNase A become active when brought together. In the late sixties, he constructed a device, first known as "Fred's folly," that helps to fit protein atomic models to experimentally derived electron maps. "Fred was an inspiring and charismatic leader, always with a great smile," adds Thomas Steitz.
Two papers look at mutations causing familial amyotrophic lateral sclerosis. One group, led by the University of Massachusetts' Robert Brown, found a cluster on chromosome 16 through loss-of-heterozygosity mapping of a family with a history of ALS. That cluster included the FUS/TLS gene and by sequencing this region in ALS families, researchers found 13 mutations, the most common ones being R521C and R521G. The other group, led by King's College London's Christopher Shaw, screened people with familial ALS to look for mutations in the FUS gene, finding two missense mutations, including R521C.
Kevin White and his colleagues made a large-scale functional network of Drosophila melanogaster of the homeobox transcription factors Even-skipped and Fushi tarazu, which are important in segmentation. From this model, they determined that the ubiquitin E3 ligase complex factor SPOP, a target of those transcription factors, mediates Jun kinase phosphatase Puckered's degradation and brings about TNF/Eiger–dependent apoptosis. In humans, SPOP is highly expressed in clear cell renal cell carcinomas.