Transplant experiments on growth and mortality of the fan mussel Pinna bicolor

Growth and mortality for different size classes (30-49 mm, 50-79 mm and 80-100 mm shell width) of the fan mussel Pinna bicolor transplanted at open sea bottom, within enclosure cages, and on suspended rafts were studied and compared over an 18-month study period. Growth, in terms of shell width, dry tissue weight and condition index of the same size class, did not show significant differences (P > 0.05) between the transplanted populations at the open sea bottom and in enclosure cages. Fastest growth was noted for the small-size class during the initial 12-month period, with a net increase in maximum shell width of 50-60 mm (100-120 mm shell length). Thereafter, growth tended to slow down and all growth parameters became similar for all the three size classes. In comparison of the small-size fan mussels between the bottom (open and caged) transplants and that on the suspended rafts, a better growth result was registered in the suspended raft population possibly due to a faster induced flow and availability of food in the water column. Mortality of transplanted P. bicolor was the highest at open sea bottom, and predominantly caused by predation by fish and crabs. Highest mortality was also noted in the small-size class as the larger fan mussels were less vulnerable to predation than the small juvenile. The number of transplanted P, bicolor at open sea bottom fell to the same natural density within the fast 12 months of the study and stabilized afterwards, suggesting that the natural population of P. bicolor was controlled by its predators. In rearing of fan mussels, both growth and mortality should be considered in concert, so as to select an optimal size class of transplants which would attain the maximum growth, with minimum mortality, over the culture period.link_to_subscribed_fulltex

Angiogenesis selectively requires the p110 alpha isoform of PI3K to control endothelial cell migration

Phosphoinositide 3-kinases (PI3Ks) signal downstream of multiple cell-surface receptor types. Class IA PI3K isoforms1 couple to tyrosine kinases and consist of a p110 catalytic subunit (p110α, p110β or p110δ), constitutively bound to one of five distinct p85 regulatory subunits. PI3Ks have been implicated in angiogenesis(2,3,4,5), but little is known about potential selectivity among the PI3K isoforms and their mechanism of action in endothelial cells during angiogenesis in vivo. Here we show that only p110α activity is essential for vascular development. Ubiquitous or endothelial cell-specific inactivation of p110α led to embryonic lethality at mid-gestation because of severe defects in angiogenic sprouting and vascular remodelling. p110α exerts this critical endothelial cell-autonomous function by regulating endothelial cell migration through the small GTPase RhoA. p110α activity is particularly high in endothelial cells and preferentially induced by tyrosine kinase ligands (such as vascular endothelial growth factor (VEGF)-A). In contrast, p110β in endothelial cells signals downstream of G-protein-coupled receptor (GPCR) ligands such as SDF-1α, whereas p110δ is expressed at low level and contributes only minimally to PI3K activity in endothelial cells. These results provide the first in vivo evidence for p110-isoform selectivity in endothelial PI3K signalling during angiogenesis