Planning your every move: the role of ß-actin and its post-transcriptional regulation in cell motility.

Cell motility is a tightly regulated process that involves the polymerization of actin subunits. The formation of actin filaments is controlled through a variety of protein factors that accelerate or perturb the polymerization process. As is the case for most biological events, cell movement is also controlled at the level of gene expression. Growing research explains how the ß-actin isoform of actin is particularly regulated through post-transcriptional events. This includes the discovery of multiple sites in the 3' untranslated region of ß-actin mRNA to which RNA-binding proteins can associate. The control such proteins have on ß-actin expression, and as a result, cell migration, continues to develop, and presents a thorough process that involves guiding an mRNA out of the nucleus, to a specific cytosolic destination, and then controlling the translation and decay of this message. In this review we will provide an overview on the recent progress regarding the mechanisms by which actin polymerization modulates cell movement and invasion and we will discuss the importance of post-transcriptional regulatory events in ß-actin mediated effects on these processes.

Metabolic and heart rate responses to hypoxia in early chicken embryos in the transition from diffusive to convective gas transport.

Measurements of normoxic, hypoxic (15% or 10% O2) and post-hypoxic oxygen consumption (VO2) were conducted in chicken embryos every other day between embryonic day 3 (E3) and day 19 (E19), out of a total embryogenic period of 20.5 days. The results indicated that, irrespective of age, hypoxia lowered VO2 throughout embryogenesis without any contraction of an O2 debt. Hypoxic hypometabolism was more prominent at E3 than at E5, probably because of the differences in O2 sensitivity during the developmental transition from O2 diffusion to O2 convection forms of gas transport. Further measurements at these two ages with either progressively increasing hypoxia or a sudden drop to 8% O2 indicated that, at E5, the less pronounced hypometabolism was accompanied by a greater drop in heart rate (HR) than at E3. It was postulated that a functional causative link existed between these two phenomena, the decrease in whole-embryo [Formula: see text] favouring O2 availability to the heart. Indeed, when O2 demands were decreased by cold exposure, the hypoxic effects on HR became similar between E3 and E5. We conclude that hypometabolism with no major reliance on anaerobic sources is the common response to hypoxia throughout embryogenesis. In the earliest phases of embryogenesis, when diffusion is the primary form of gas transport and despite the absence of neural regulation, the possibility of using some of the O2 saved in favour of the heart adds further value to hypometabolism as a survival strategy against hypoxia.