"How Transcription Factors Program Chromatin during Hematopoietic Development: Lessons from Myeloid-specific Genes" Constanze Bonifer, Division of Experimental Haematology, University of Leeds, UK.

Karl Deisseroth, associate professor of bioengineering, Stanford University.

Researchers at Caltech have shown that a highly specific intrabody (an antibody fragment that works against a target inside a cell) is capable of stalling the development of Huntington's disease in a variety of mouse models. "Gene therapy in these models successfully attenuated the symptoms of Huntington's disease and increased life span," notes Paul Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences.

Researchers at Caltech have proposed a novel model that differs from a widely held hypothesis about the mechanisms by which developing animals pattern their tissues and structures. Cells in a developing animal require information about their position with respect to other cells so that they can adopt specific patterns of gene expression and function correctly. The most accepted paradigm is that this positional information comes in the form of chemical signals called morphogens; morphogens are differentially distributed across the developing field, with cells acquiring the information about their position relative to their neighbors by "measuring" and interpreting the local concentrations of the morphogen.