The 2015 landslide and tsunami in Taan Fiord, Alaska.

Glacial retreat in recent decades has exposed unstable slopes and allowed deep water to extend beneath some of those slopes. Slope failure at the terminus of Tyndall Glacier on 17 October 2015 sent 180 million tons of rock into Taan Fiord, Alaska. The resulting tsunami reached elevations as high as 193 m, one of the highest tsunami runups ever documented worldwide. Precursory deformation began decades before failure, and the event left a distinct sedimentary record, showing that geologic evidence can help understand past occurrences of similar events, and might provide forewarning. The event was detected within hours through automated seismological techniques, which also estimated the mass and direction of the slide - all of which were later confirmed by remote sensing. Our field observations provide a benchmark for modeling landslide and tsunami hazards. Inverse and forward modeling can provide the framework of a detailed understanding of the geologic and hazards implications of similar events. Our results call attention to an indirect effect of climate change that is increasing the frequency and magnitude of natural hazards near glaciated mountains.

Histone H3.3 is enriched in covalent modifications associated with active chromatin.

Chromatin states can be distinguished by differential covalent modifications of histones or by utilization of histone variants. Chromatin associated with transcriptionally active loci becomes enriched for histones with particular lysine modifications and accumulates the H3.3 histone variant, the substrate for replication-independent nucleosome assembly. However, studies of modifications at particular loci have not distinguished between histone variants, so the relationship among modifications, histone variants, and nucleosome assembly pathways is unclear. To address this uncertainty, we have quantified the relative abundance of H3 and H3.3 and their lysine modifications. Using a Drosophila cell line system in which H3.3 has been shown to specifically package active loci, we found that H3.3 accounts for approximately 25% of total histone 3 in bulk chromatin, enough to package essentially all actively transcribed genes. MS and antibody characterization of separated histone 3 fractions revealed that H3.3 is relatively enriched in modifications associated with transcriptional activity and deficient in dimethyl lysine-9, which is abundant in heterochromatin. To explain enrichment on alternative variants, we propose that histone modifications are tied to the alternative nucleosome assembly pathways that use primarily H3 at replication forks and H3.3 at actively transcribed genes in a replication-independent manner.

Mathematical models of RNA silencing: unidirectional amplification limits accidental self-directed reactions.

RNA silencing, found broadly throughout the eukaryotes, posttranscriptionally suppresses the expression of "aberrant" genes including those of many viruses and transposons. Similar to the specific immune system of vertebrates, RNA silencing works by generating specific responses against foreign elements and rapidly amplifying these responses to clear or otherwise inactivate the threat. Also like the vertebrate immune system, RNA-silencing systems risk making mistakes and mounting undesirable responses against the self. We develop a set of mathematical models of RNA silencing. We show that current models of RNA silencing do little to explain what prevents mistaken reactions from silencing vital organismal genes. We extend the basic models to show that the presumed unidirectional nature of the amplification process (namely, unidirectional RNA-directed RNA polymerase-mediated synthesis of secondary double-stranded RNA as observed in Caenorhabditis elegans) serves as a "safety mechanism" that safeguards against accidental generation of damaging self-directed reactions.