Michael Abercrombie: contact inhibition of locomotion and more

Michael Abercrombie is regarded as one of the principal pioneers of cell biology. Although Abercrombie began his career as an experimental embryologist, working on the avian organizer with C. H. Waddington, questions on how cells in culture migrate and interact dominated his career. Whilst studying the social behaviour of chick heart embryonic fibroblasts, Abercrombie identified a phenomenon whereby colliding cells collapse their protrusions towards the cell-cell contact upon a collision, preventing their continued migration. The cells then form protrusions away from the contact and, space permitting, migrate away from each other. This behaviour is now referred to as ‘contact inhibition of locomotion’ and has been identified within embryology as the driving force behind the directional migration of the neural crest and the dispersion patterning of haemocytes and Cajal-Retzius neurons. Furthermore, its loss between collisions of cancer cells and healthy cells is associated with metastasis. In this review we begin with an overview of Abercrombie’s life and highlight some of his key publications. We then discuss Abercrombie’s discovery of contact inhibition of locomotion, the roles which cell-cell adhesions, cell-matrix adhesions and the cytoskeleton play in facilitating this phenomenon, and the importance of contact inhibition of locomotion within the living organism

Redistribution of Adhesive Forces through Src/FAK Drives Contact Inhibition of Locomotion in Neural Crest

Contact inhibition of locomotion is defined as the behavior of cells to cease migrating in their former direction after colliding with another cell. It has been implicated in multiple developmental processes and its absence has been linked to cancer invasion. Cellular forces are thought to govern this process; however, the exact role of traction through cell-matrix adhesions and tension through cell-cell adhesions during contact inhibition of locomotion remains unknown. Here we use neural crest cells to address this and show that cell-matrix adhesions are rapidly disassembled at the contact between two cells upon collision. This disassembly is dependent upon the formation of N-cadherin-based cell-cell adhesions and driven by Src and FAK activity. We demonstrate that the loss of cell-matrix adhesions near the contact leads to a buildup of tension across the cell-cell contact, a step that is essential to drive cell-cell separation after collision

Transfer printing of AlGaInAs/InP etched facet lasers to Si substrates

InP-etched facet ridge lasers emitting in the optical C-band are heterogeneously integrated on Si substrates by microtransfer printing for the first time. 500 μm × 60 μm laser coupons are fabricated with a highly dense pitch on the native InP substrate. The laser epitaxial structure contains a 1-μm-thick InGaAs sacrificial layer. A resist anchoring system is used to restrain the devices while they are released by selectively etching the InGaAs layer with FeCl3:H2O (1:2) at 8 °C. Efficient thermal sinking is achieved by evaporating Ti-Au on the Si target substrate and annealing the printed devices at 300 °C. This integration strategy is particularly relevant for lasers being butt coupled to polymer or silicon-on-insulator (SOI) waveguides

Studying the Low-Income Family

How do low-income farm families perceive poverty and do they relate themselves to it? Are they satisfied with their present condition? Are they willing to change? In an attempt to answer these questions and gain knowledge about the economic, social, and psychological factors that facilitate or hinder change, a study was made of families in a low-farm-income area of Wisconsin. Findings are discussed and suggestions made for Extension personnel working with low-income families

Comparison of InGaAs and InAlAs sacrificial layers for release of InP-based devices

Heterogeneous integration of InP devices to Si substrates by adhesive-less micro transfer printing requires flat surfaces for optimum attachment and thermal sinking. InGaAs and InAlAs sacrificial layers are compared for the selective undercut of InP coupons by FeCl3:H2O (1:2). InAlAs offers isotropic etches and superior selectivity (> 4,000) to InP when compared with InGaAs. A 500 nm thick InAlAs sacrificial layer allows the release of wide coupons with a surface roughness < 2 nm and a flatness < 20 nm. The InAlAs release technology is applied to the transfer printing of a pre-fabricated InP laser to a Si substrate

The role and regulation of cell matrix adhesions during contact inhibition of locomotion

Contact inhibition of locomotion (CIL) was first characterised over 60 years ago and defined as the behaviour of a cell to cease its continued migration in the same direction upon a collision with another cell. It has been implicated in multiple developmental processes including the precise dispersion of haemocytes and the directional migration of the cranial neural crest. In addition its absence has been linked to metastasis in cancer. Although many molecular mechanisms have recently been implicated in CIL, the role of cell-matrix adhesions (CMAs) during this process remains unknown. It has been hypothesised that cellular forces play an important role in CIL; however the role of traction forces generated via CMAs and intercellular tension during CIL is unclear. In this present study neural crest cells are used to elucidate the role and regulation of CMAs during CIL. The findings presented here demonstrate a rapid disassembly of CMAs near the cell-cell contact between colliding cells. This disassembly is shown to be dependent upon the formation of N-cadherin based cellcell adhesions and driven by Src and FAK kinase activity. Furthermore this rapid disassembly of CMAs during CIL leads to a redistribution of intercellular forces from the substrate to the cell-cell contact and is essential to drive cell-cell separation after a collision

Notes on a scandal: the official enquiry into deviance and corruption in New Zealand police

Since 2004, the New Zealand Police Service has been engulfed by a series of scandals relating to allegations that officers have committed rape and sexual assault and conducted inappropriate sexual relations with vulnerable people. Moreover, it has been claimed that other officers engaged in corrupt practices to thwart the investigation and prosecution of criminal behaviour of police officers. In 2007, a Commission of Inquiry report established a program of reform intended to shape the future direction of the police service. This article provides an overview of these scandals, the context in which they have emerged, and the political and policing response to them. The analysis contained in the Commission report is compared with that offered by comparable investigations of police deviance and corruption in other countries. The methodological and conceptual limitations of the Commission are outlined and the prospects of the recommendations are considered

Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw.

The amniote jaw complex is a remarkable amalgamation of derivatives from distinct embryonic cell lineages. During development, the cells in these lineages experience concerted movements, migrations, and signaling interactions that take them from their initial origins to their final destinations and imbue their derivatives with aspects of form including their axial orientation, anatomical identity, size, and shape. Perturbations along the way can produce defects and disease, but also generate the variation necessary for jaw evolution and adaptation. We focus on molecular and cellular mechanisms that regulate form in the amniote jaw complex, and that enable structural and functional integration. Special emphasis is placed on the role of cranial neural crest mesenchyme (NCM) during the species-specific patterning of bone, cartilage, tendon, muscle, and other jaw tissues. We also address the effects of biomechanical forces during jaw development and discuss ways in which certain molecular and cellular responses add adaptive and evolutionary plasticity to jaw morphology. Overall, we highlight how variation in molecular and cellular programs can promote the phenomenal diversity and functional morphology achieved during amniote jaw evolution or lead to the range of jaw defects and disease that affect the human condition