In this week's PNAS Early Edition, a pair of researchers at Israel's Tel Aviv University and Bar Ilan University propose that the "lateral acquisition of genes is affected by the friendliness of their products." Uri Gophnaa and Yanay Ofranb say genes that encode proteins involved in multiple protein-protein interactions "have a greater chance of forming new interactions in new species" and may "be more prone to transfer than genes with fewer interactions." The pair says that their proposal overcomes the challenge that evolutionary constraints have conferred in previous lateral gene acquisition theories.
Researchers at the University of Texas Health Science Center in San Antonio show that in a mouse model of Alzheimer's disease, CREB-binding protein gene transfer "increases [brain-derived neurotrophic factor] levels and ameliorates learning and memory deficits." More specifically, the team shows that amyloid-β accumulation-induced learning and memory impairments "are mediated by alterations in CREB function," and that therefore, inducing CBP expression may be a "valid therapeutic approach" for Alzheimer's and other "brain disorders characterized by alterations in immediate early genes."
In another PNAS paper published online in advance, researchers at the University of Chicago, along with their collaborators at the National Institute of Environmental Health Sciences, show that "SIRT1 acts as a tumor suppressor through its role in DNA repair." As a result of DNA damage, SIRT1 enhances the expression of the xeroderma pigmentosum C protein, which is critical to initiate nucleotide excision repair "by reducing AKT-dependent nuclear localization of the transcription repressor of XPC." The team also found "significantly reduced" levels of SIRT1 in skin tumors from Caucasian patients.
Duke University's Shui Wang et al. report that in Arabidopsis, brca1 and rad51 are "hyper-susceptible not only to genotoxic substances, but also to pathogen infections." In their whole-genome microarray analysis, the Duke researchers found that "downstream of NPR1, BRCA2A is a major regulator of defense-related gene transcription," and that "RAD51 is specifically recruited to the promoters of defense genes during [systemic acquired resistance]." Wang et al. write that their investigations revealed that the BRCA2–RAD51 complex, which is known for its role in homologous recombination, "also plays a direct and specific role in transcription regulation during plant immune responses."