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Parkinson’s disease-associated LRRK2 kinase is recruited to membranes by its Rab GTPase substrates, and LRRK2 is both retained on membranes and further activated there by cooperative interaction with the phosphorylated Rab proteins that it generates.

The brain and olfactory epithelium play a key role in pattering chondrogenic areas in the developing face, which is partly based on the release of SHH from neurosensory structures into the facial mesenchyme.

The Hox transcription factor Ultrabithorax (Ubx) represses alternative gene programs during lineage development by lineage-specific Polycomb protein complex retention at Ubx-targeted chromatin sites.

Unbiased functional proteomics reveal that protein interactions are a key regulator of the strength of synaptic inhibition in neurons of the central nervous system.

The mechanistic impact of genetic variants can be combined with previous knowledge on gene function to deliver conditional growth predictions and pave the way for personalized genetic interventions.

The strength of TCR signalling determines the rate at which cells initiate a tightly coordinated signalling programme, without altering its organization.

A massively parallel analysis of the effects of mutations on amyloid beta nucleation provide the first comprehensive atlas of how mutations alter the formation of amyloid fibrils.

Nuclear pores assemble asymmetrically, by an inside-out evagination of the inner nuclear membrane that grows in diameter and depth until it fuses with the flat outer nuclear membrane.

Improved characterisation of human embryonic lung development highlights human-mouse differences and facilitates the development of defined culture conditions for the expansion of self-renewing, multipotent human lung epithelial progenitor cells.

A near-complete flux balance analysis model of a minimal cell demonstrates the high essentiality of its metabolic genes, agrees well with experimental essentiality data and suggests some further gene removals.