Research Highlights in 2015

The suppression of homologous recombination in G1 depends on BRCA1–PALB2–BRCA2 complex formation at sites of damage. In mitosis, DNA repair factors prevent the formation of DNA damage by facilitating mitotic replication.

Centrosomes can nucleate not only microtubules but also actin filaments, in a process dependent on the actin-related protein 2/3 complex and WASH.

Cytoplasmic, but not nuclear, aggregates of β-sheet proteins mediate toxic effects through impaired nucleo-cytoplasmic transport of mRNA and protein.

The ubiquitin ligase COP1 promotes insulin secretion in mice by inducing the degradation of transcription factors ETV1, ETV4 and ETV5.

The primase–polymerase PrimPol is required for bypassing G-quadruplexes in vertebrate cells by repriming replication downstream of the structures.

Cep135, Ana1 (Cep295) and Asterless (Cep152) are sequentially recruited to daughter centrioles to enable their maturation into duplication-competent mother centrioles.

Two studies provide novel insights into how the Dpp morphogen regulates fly wing growth.

Analyses ofDrosophila melanogasterpolytene chromosomes elucidate the interconnections between gene expression, genome organization into topologically associated domains (TADs) and the structures of euchromatin and heterochromatin.

Autophagy-induced degradation of the nuclear lamina protects cells from tumorigenesis

The Hippo signalling pathway regulates spindle orientation and asymmetric cell division

A novel protocol for protein interactome analysis in three dimensions identifies the crucial role of highly abundant, weak interactions.

Sestrin 2 has been shown to function as a leucine sensor for the mTORC1 signalling pathway.

Transgenic plants expressing viral DNA-targeting components of the CRISPR–Cas genome editing system are immune to geminiviruses.

The DNA damage response kinase ATR has an anti-apoptotic role in mitochondria.

DNA damage repair is in the spotlight this year — the Nobel Prize in Chemistry 2015 was awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar “for mechanistic studies of DNA repair”.

The ubiquitylation enzyme cullin 3 and its adaptor KBTBD8 mediate stem cell specification into neural crest by modulating the translation of a specific set of mRNAs.

Current research illustrates that various proteins, implicated in both physiological and pathological processes, can undergo phase separation to form liquid droplets.

A feedback loop involving non-muscle myosin II and Rho-associated protein kinase I provides a robust mechanism for stabilizing epithelial junctions.

The 2015 Lasker Award for Basic Medical Research goes to E. Witkin and S. Elledge for their studies on DNA damage response pathways.