Disordered hinge regions of the AP-3 adaptor complex promote vesicle budding from the late Golgi in yeast.

Vesicles bud from maturing Golgi cisternae in a programmed sequence. Budding is mediated by adaptors that recruit cargoes and facilitate vesicle biogenesis. In Saccharomyces cerevisiae, the AP-3 adaptor complex directs cargoes from the Golgi to the lysosomal vacuole.

Data on the effects of ECM rigidity on actomyosin contractility and invadopodia activity in individual versus pairs of head and neck squamous cell carcinoma cells.

Migration through the extracellular matrix (ECM) is essential for cancer cells to escape the primary tumor and invade neighboring tissues with the potential for metastasis [1]. To penetrate tissue barriers, migrating cancer cells degrade the ECM with actin-rich membrane protrusions called invadopodia [2]. We have previously found that invadopodial ECM degradation is regulated by ECM rigidity in a process mediated by contractile forces in individual head and neck squamous cell carcinoma (HNSCC) cells [3], [4].

Bro1 binds the Vps20 subunit of ESCRT-III and promotes ESCRT-III regulation by Doa4.

The budding of intralumenal vesicles (ILVs) at endosomes requires membrane scission by the ESCRT-III complex. This step is negatively regulated in yeast by Doa4, the ubiquitin hydrolase that deubiquitinates transmembrane proteins sorted as cargoes into ILVs. Doa4 acts non-enzymatically to inhibit ESCRT-III membrane scission activity by directly binding the Snf7 subunit of ESCRT-III.

Data on the mechanobiological differences in the transcriptomes of human fetal and adult dermal fibroblasts in response to extracellular matrix rigidity.

Fetal skin is known to proceed through the wound healing process without the formation of scar tissue but rather via regeneration. Fetal dermal fibroblasts have emerged as a significant driving force in this regenerative response due to their unique phenotypic characteristics including our recent finding of an attenuated contractile response to extracellular matrix (ECM) rigidity that normally contributes to myofibroblast differentiation and scar formation. We provide data here that these mechanobiological differences in fetal dermal fibroblasts also extend to their genetic profile in which we found 353 differentially expressed genes when compared to adult dermal fibroblasts.

The altered mechanical phenotype of fetal fibroblasts hinders myofibroblast differentiation.

During the dermal wound healing process, the mechanical rigidity of the newly deposited extracellular matrix and transforming growth factor-β1 promote the transition of fibroblasts into myofibroblasts. Myofibroblasts generate large cellular forces that contract and remodel the extracellular matrix leading to scar formation. In contrast, myofibroblasts are not detected in fetal dermal wounds which are more compliant and contain less transforming growth factor-β1 than adult wounds.

The ROCK isoforms differentially regulate the morphological characteristics of carcinoma cells.

Rho-associated kinase (ROCK) activity drives cell migration via actomyosin contractility. During invasion, individual cancer cells can transition between 2 modes of migration, mesenchymal and amoeboid. Changes in ROCK activity can cause a switch between these migration phenotypes which are defined by distinct morphologies.