Acquisition of Animal Gene by Horizontal Transfer
University of Ottawa ♦ University of British Columbia ♦ University of Illinois ♦ Albert Einstein College of Medicine
Published in Current Biology (Cell Press), August 9, 2011
Researchers have recently made a rather surprising discovery — an animal gene that appears to have been taken up by the microsporidian Encephalitozoon romaleae. This is the first time that an animal gene has been documented in a microsporidian genome. Microsporidians often parasitise arthropods, and have been known to take up foreign DNA from bacteria through a process known as horizontal gene transfer. New DNA allows microsporidians to gain new functions that promote survival. After carrying out a screen of the microsporidian genome they found but one candidate animal gene, which was identified as a purine nucleotide phosphorylase (PNP). Phylogenetic analysis later revealed that the gene was likely of arthropod origin and could have been taken up by E. romaleae after it parasitised an insect.
Genetics Underpinning ALS
University of Montreal ♦ Published in PLoS Genetics, August 4, 2011
Using the zebrafish as a model, researchers have elucidated the connection between some of the common mutations associated with amyotrophic lateral sclerosis (ALS). Mutations in the genes SOD1 and TARDBP have been known to cause ALS, as has a mutation in the Fused in sarcoma gene (FUS). In this study researchers show that mutations in the FUS gene cause a loss of function; they cannot rescue the motor phenotype caused by a knockdown of the zebrafish Fus gene. It seems that the FUS and TARDBP mutations share a common pathogenic mechanism, as there co-expression did not exacerbate the phenotype observed when either were expressed alone. Findings indicate that SOD1 works through a second distinct mechanism however, as wildtype SOD1 was unable to rescue the phenotype observed after overexpression of FUS and TARDBP mutations.
Balancing Host Defense and Wound Repair
University of Toronto ♦ Hospital for Sick Children ♦ Benaroya Research Institute ♦ University Hospital Erlangen
Published in Immunity (Cell Press), August 3, 2011
Tak Mak’s lab provides some new insights into the mechanism by which thymic stromal lymphopoietin (TSLP) modulates the immune system in order to curb inflammation and launch the healing process in the colon. Using a knockout mouse model researchers illustrate that the absence of TSLP does not increase the severity of colitis, but instead prevents healing and recovery from the disease. Mice without the TSLP gene exhibited increased concentrations of an enzyme known as neutrophil elastase and decreased expression of secretory leukocyte peptidase inhibitor (SLPI). Typically SLPI serves to stomp out some of the immune response following insult to the colon by acting as a serine protease inhibitor and inhibitor of NF-κB. In the absence of TLSP signaling, however, it seems SLPI is downregulated, preventing mucosal healing.