Analysis of knockout and knockdown melanoma cells and TCGA melanoma data shows that the microphthalmia-associated transcription factor (MITF) is a major repressor of extracellular matrix (ECM) and focal adhesion genes.

The PBAF chromatin-remodelling complex is essential for the proliferation of melanocytes and melanoma cells and is recruited to critical regulatory elements by physical and functional interactions with MITF, a transcription factor and master regulator of melanoma.

A comprehensive, quantitative, protein-protein interaction screen maps the network of interactions between human MIT domains and ESCRT-III C-terminal tails, and reveals MIT domain-containing protein cofactors for abscission and the 'No Cut' abscission checkpoint.

A combination of functional, biochemical and imaging studies show that LINE-1/L1 proteins and mRNA enter the nucleus through mitotic nuclear membrane breakdown, interact with components of the DNA replication fork and mediate retrotransposition during S phase.

ULK3 is a kinase in the abscission checkpoint that temporarily inactivates ESCRT-III proteins via phosphorylation, which is required to delay cytokinesis in response to defects in mitosis.

Impaired nuclear import of the transcription factor TFEB/MITF is a major cause of autophagy and lysosome dysfunction in amyotrophic lateral sclerosis caused by mutations in the C9orf72 gene.

The oncogenic role ligand-dependent BMP signaling plays in suppressing differentiation in melanoma is a reiteration of its physiological roles during melanocyte development.

G-actin binding controls the susceptibility of MRTF-A to phosphorylation, which works in concert with multiple NES elements to regulate MRTF-A subcellular localisation and activity.

A genetic discovery screen for epigenetic factors accelerating melanoma development in vivo identifies SATB2 as a driver of tumor invasion and resistance to FDA-approved BRAF-targeted inhibitor Vemurafenib.

Zebrafish pigment cell progenitors are a heterogeneous class of adult tissue-resident cells which reiterate developmental signaling during melanocyte regeneration.