Rootless cone eruption processes informed by dissected tephra deposits and conduits

Rootless cones result from the explosive interaction between lava flows and underlying water-saturated sediment or volcaniclastic deposits. Rootless explosions can represent a significant far-field hazard during basaltic eruptions, but there are few detailed studies of their deposits. A rootless cone field in the 8.5 Ma Ice Harbor flow field of the Columbia River Basalt Province, NW USA, is revealed by sections through rootless conduit and cone structures. The Ice Harbor lava flow hosting the rootless cones was emplaced across a floodplain or lacustrine environment that had recently been mantled by a layer of silicic volcanic ash from a major explosive eruption. Our observations indicate a two-stage growth model for the rootless cones: (1) initial explosions generated sediment-rich tephra emplaced by fallout and pyroclastic density currents and (2) later weaker explosions that generated spatter-rich fountains. Variable explosive activity resulted in a wide range of pyroclast morphologies and vesicularities. Cross-sections through funnel-shaped conduits also show how the conduits were constructed and stabilised. The growth model is consistent with decreasing water availability with time, as inferred for rootless cones described in Iceland. The Ice Harbor rootless cones provide further lithological data to help distinguish between rootless cone-derived tephra and tephra generated above an erupting dyke

Frequent somatic mutations in MAP3K5 and MAP3K9 in metastatic melanoma identified by exome sequencing

We sequenced eight melanoma exomes to identify new somatic mutations in metastatic melanoma. Focusing on the mitogen-activated protein (MAP) kinase kinase kinase (MAP3K) family, we found that 24% of melanoma cell lines have mutations in the protein-coding regions of either MAP3K5 or MAP3K9. Structural modeling predicted that mutations in the kinase domain may affect the activity and regulation of these protein kinases. The position of the mutations and the loss of heterozygosity of MAP3K5 and MAP3K9 in 85% and 67% of melanoma samples, respectively, together suggest that the mutations are likely to be inactivating. In in vitro kinase assays, MAP3K5 1780F and MAP3K9 W333* variants had reduced kinase activity. Overexpression of MAP3K5 or MAP3K9 mutants in HEK293T cells reduced the phosphorylation of downstream MAP kinases. Attenuation of MAP3K9 function in melanoma cells using siRNA led to increased cell viability after temozolomide treatment, suggesting that decreased MAP3K pathway activity can lead to chemoresistance in melanoma