Reproductive behavior of Atlantic halibut (Hippoglossus hippoglossus) interpreted from electronic tags.

Reproductive timing, location, and behavior are important characteristics that determine marine population dynamics, structure, and resilience to threats, including fishing and climate change. It is challenging to evaluate factors driving variability in these reproductive traits in wild fishes because of the difficulty observing individuals in their natural environments. In the present study, we used high-resolution depth, temperature, and acceleration time series recorded by pop-up satellite archival tags to (1) identify and characterize patterns in depth and acceleration that may be indicative of spawning events in large Atlantic halibut (Hippoglossus hippoglossus), and (2) estimate the effects of individual traits (body size and sex) and environmental factors (location and temperature) on spawning time and frequency. Unique rapid rises observed in the winter depth profiles were interpreted as spawning events. The initiation of the first presumed spawning rise was negatively correlated to water temperature experienced during the prespawning season, suggesting that currently increasing water temperature in the Gulf of St. Lawrence may induce phenological change in halibut spawning time. The number of rises of batch-spawning females was unrelated to female body size. The present study demonstrates how electronic tagging can be used for in-depth characterization of timing, location, and behaviors associated with spawning in a large flatfish species. Such information can inform spatiotemporal management and conservation measures aiming to protect species from directed fishing and by-catch during spawning.

Down-regulation of cell surface CXCR4 by HIV-1.

BACKGROUND: CXC chemokine receptor 4 (CXCR4), a member of the G-protein-coupled chemokine receptor family, can serve as a co-receptor along with CD4 for entry into the cell of T-cell tropic X4 human immunodeficiency virus type 1 (HIV-1) strains. Productive infection of T-lymphoblastoid cells by X4 HIV-1 markedly reduces cell-surface expression of CD4, but whether or not the co-receptor CXCR4 is down-regulated has not been conclusively determined. RESULTS: Infection of human T-lymphoblastoid cell line RH9 with HIV-1 resulted in down-regulation of cell surface CXCR4 expression. Down-regulation of surface CXCR4 correlated temporally with the increase in HIV-1 protein expression. CXCR4 was concentrated in intracellular compartments in H9 cells after HIV-1 infection. Immunofluorescence microscopy studies showed that CXCR4 and HIV-1 glycoproteins were co-localized in HIV infected cells. Inducible expression of HIV-1 envelope glycoproteins also resulted in down-regulation of CXCR4 from the cell surface. CONCLUSION: These results indicated that cell surface CXCR4 was reduced in HIV-1 infected cells, whereas expression of another membrane antigen, CD3, was unaffected. CXCR4 down-regulation may be due to intracellular sequestering of HIV glycoprotein/CXCR4 complexes.