Evidence for enhanced mixing over rough topography in the abyssal ocean

The overturning circulation of the ocean plays an important role in modulating the Earth's climate. But whereas the mechanisms for the vertical transport of water into the deep ocean--deep water formation at high latitudes--and horizontal transport in ocean currents have been largely identified, it is not clear how the compensating vertical transport of water from the depths to the surface is accomplished. Turbulent mixing across surfaces of constant density is the only viable mechanism for reducing the density of the water and enabling it to rise. However, measurements of the internal wave field, the main source of energy for mixing, and of turbulent dissipation rates, have typically implied diffusivities across surfaces of equal density of only approximately 0.1 cm2 s(-1), too small to account for the return flow. Here we report measurements of tracer dispersion and turbulent energy dissipation in the Brazil basin that reveal diffusivities of 2-4 cm2 s(-1) at a depth of 500 m above abyssal hills on the flank of the Mid-Atlantic Ridge, and approximately 10 cm2 s(-1) nearer the bottom. This amount of mixing, probably driven by breaking internal waves that are generated by tidal currents flowing over the rough bathymetry, may be large enough to close the buoyancy budget for the Brazil basin and suggests a mechanism for closing the global overturning circulation.     

Mutant frizzled-4 disrupts retinal angiogenesis in familial exudative vitreoretinopathy

Familial exudative vitreoretinopathy (FEVR) is a hereditary ocular disorder characterized by a failure of peripheral retinal vascularization. Loci associated with FEVR map to 11q13-q23 (EVR1; OMIM 133780, ref. 1), Xp11.4 (EVR2; OMIM 305390, ref. 2) and 11p13-12 (EVR3; OMIM 605750, ref. 3). Here we have confirmed linkage to the 11q13-23 locus for autosomal dominant FEVR in one large multigenerational family and refined the disease locus to a genomic region spanning 1.55 Mb. Mutations in FZD4, encoding the putative Wnt receptor frizzled-4, segregated completely with affected individuals in the family and were detected in affected individuals from an additional unrelated family, but not in normal controls. FZD genes encode Wnt receptors, which are implicated in development and carcinogenesis. Injection of wildtype and mutated FZD4 into Xenopus laevis embryos revealed that wildtype, but not mutant, frizzled-4 activated calcium/calmodulin-dependent protein kinase II (CAMKII) and protein kinase C (PKC), components of the Wnt/Ca(2+) signaling pathway. In one of the mutants, altered subcellular trafficking led to defective signaling. These findings support a function for frizzled-4 in retinal angiogenesis and establish the first association between a Wnt receptor and human disease.