The mutational landscape of lethal castration-resistant prostate cancer

Grasso, C.S. et al. Nature doi:10.1038/nature11125 (20 May).

Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer

Barbieri, C.E. et al. Nat. Genet. 44, 685–689 (2012).

Two studies use exome sequencing to investigate the genetic basis of prostate cancer. Barbieri et al. identify recurrent mutations in multiple genes in prostate cancer, showing that SPOP contains the most frequent recurrent mutations. Grasso et al. define mutations in castration-resistant prostate cancer, suggesting a mechanism through which these cancers become resistant to antiandrogen therapy.

F-box protein FBXL19–mediated ubiquitination and degradation of the receptor for IL-33 limits pulmonary inflammation

Zhao, J. et al. Nat. Immunol. doi:10.1038/ni.2341 (3 June).

The cytokine IL-33 is important in lung inflammatory conditions such as asthma. The interaction between IL-33 and its receptor ST2L is shown to be regulated by an intracellular protein FBXL19, which binds and degrades ST2L. Therapeutic modulation of this axis might be one way to reduce lung inflammation.

Autism spectrum disorder susceptibility gene TAOK2 affects basal dendrite formation in the neocortex

Calderon de Anda, F. et al. Nat. Neurosci. doi:10.1038/nn.3141 (10 June).

The authors find that the gene encoding thousand-and-one amino acid 3 kinase (TAOK2), which has been associated with susceptibility to autism spectrum disorders, is essential for dendrite morphogenesis. They also define a pathway involving TAOK2, neuropilin 1, semaphorin 3A and JNK that regulates the development of basal dendrites in the cortex.

Structural basis of evasion of cellular adaptive immunity by HIV-1 Nef

Jia, X. et al. Nat. Struct. Mol. Biol. doi:10.1038/nsmb.2328 (17 June).

The authors characterize the structure of a complex of the HIV-1 restriction factor Nef, the class I major histocompatibility complex and a subunit of the clathrin adaptor protein complex 1. This allowed them to show how Nef can modulate host membrane trafficking, enabling HIV-1 to evade the adaptive immune system.