In the early online edition of PNAS this week, scientists have used a screening technique to find a dual role for the methyltransferase G9a in regulating β-globin transcription. Led by senior author, Marjorie Brand at the Ottawa Hospital Research Institute, they used a proteomics screen to identify G9a as an interacting partner of the hematopoietic activator NF-E2, and that G9a is recruited to the β-globin locus by this partner. "Collectively, these results reveal a dual role for G9a in maintaining proper expression (both repression and activation) of the β-globin genes in differentiating adult erythroid cells," they write.
Taiwanese scientists studied how glycans on influenza hemagglutinin affect receptor binding and immune response. Viral transmission, they write, happens when hemagglutinin (HA) glycoprotein, which is on the viral coat of influenza, and sialic acid (SA) containing glycans, which are on the host cell surface, interact. To test which glycans might be important, they built a synthetic SA microarray and measured the binding affinity and specificity of different HA glycoforms. They found that "truncation of the N-glycan structures on HA increased SA binding affinities while decreasing specificity toward disparate SA ligands."
Takeshi Isoda of Tokyo Medical and Dental University and Anthony Ford at Institute of Cancer Research in the UK have proved that mother to offspring transmission of a single cell clone can occur in cancer. In this study they used genetic information to show that maternal and infant cancer clones in leukemia share the same unique BCR-ABL1 genomic fusion sequence, "indicating a shared, single-cell origin," they write. Microsatellite markers in the infant cancer were all of maternal origin, too.
A paper from Silvana Paredes and Keith Maggert at Texas A&M University has found a connection between heterochromatin and rDNA. Deleting a series of rDNA genes, which are highly organized, in the Drosophila Y chromosome, they show that this resulted in "reduced heterochromatin-induced gene silencing elsewhere in the genome, and the extent of the rDNA deletion correlates with the loss of silencing."