Malaria parasites avoid destruction by their host's immune response through systematic and coordinated expression switching between members of a network of variant antigen-encoding genes, a process that is mediated by a uniquely conserved gene called var2csa.

Increased expression of Drosophila Tailless (TLX homologue) reverts intermediate progenitors to neural stem cells, inducing tumourigenesis via Asense repression and reflecting mutually exclusive TLX and ASCL1 expression in human glioblastoma.

The recently characterized opsin group of xenopsins is likely a major player in animal eye evolution and may have been present in an ancient, highly plastic eye photoreceptor cell type.

In neocortex, Nav1.1 is expressed in neocortical pyramidal tract projection neurons and a minor subpopulation of cortico-cortical projection neurons in addition to its predominant expression in inhibitory neurons, while the majority of cortico-thalamic, cortico-striatal, and cortico-cortical neurons express Nav1.2.

Lmo4 specifies two neuron subclasses in the mouse neocortex by promoting postnatal co-expression of the transcription factors Ctip2 and Satb2 via chromatin remodelling in a time and area-specific manner.

The first comprehensive analysis of antigenic switching in the malaria-causing parasite Plasmodium falciparum provides new insights into the process that prevents individuals from acquiring immunity to the disease.

Co-mutation of two powerful oncogenes in certain cell types may have a lethal effect that explains the mutual exclusivity of the mutations.

The dorsal telencephalon (pallium) in medaka fish accommodates an epigenetically distinct brain area that selectively regulates unique set of synaptic genes compared to the surrounding pallial region, providing insights into the evolution of the pallium in vertebrate.

SF3B1-K700E, a gene mutaiton found recurrently mutated in pancreatic cancer, increases malignancy in an autochthonous mouse model of pancreatic cancer and induces resistance against TGF-β-induced apoptosis in vitro by missplicing of MAP3K7.

Biochemical and genetic experiments show that Ebf and Lhx2 cooperate to specify olfactory receptor enhancers, which cooperate to drive olfactory receptor expression.