In a paper appearing in this week's PNAS Early Edition, researchers at Duke University, China's Tsingua University, and at Sage Bionetworks in Seattle identify "type II cells, Clara cells in the terminal bronchioles, and putative bronchoalveolar stem cells as cells of origin for K-Ras-induced lung hyperplasia." The team also reports that of these, "only type II cells appear to progress to adenocarcinoma."
Investigators in France and Japan this week show that the Drosophila homolog of human myeloid leukemia factor 1 controls the homeostasis of the fruit fly's hematopoietic system. "Notably, mlf participates in a positive feedback loop to fine tune the activity of the RUNX transcription factor Lozenge during development of the crystal cells, one of the two main blood cell lineages in Drosophila," the authors write. In the human leukemic blood cell line Kasumi-1, the team shows that "MLF1depletion impairs RUNX1-ETO accumulation and reduces RUNX1-ETO-dependent proliferation."
Elsewhere in this week's Early Edition, investigators at Germany's Ulm University report on a family of multiple organellar RNA editing factor, or MORF, proteins, which the authors say provide "additional components of the RNA editing machinery in both" plastids and mitochondria. The team specifically identifies two MORF proteins required for editing in plastids, and points to others essential for editing in mitochondria. "The loss of a MORF protein abolishes or lowers editing at multiple sites, many of which are addressed individually by PPR proteins," the authors write.