?).Peebles: expect surprises and think outside the box yes! #aas228 Kevin Schawinski (@kevinschawinski) June 15, 2016His comparison of local vs. high-redshift cosmology in terms of scales of problems was outstanding, and he encouraged the audience and the community to keep an open mind. After all, in Sean Carrolls words, we do live in a preposterous universe, and the time is almost right to explain it all.This The Limits of Scientific Cosmology series at #aas228 has been absolutely fantastic. @AAS_Office please put videos on youtube! Kevin Schawinski (@kevinschawinski) June 15, 2016Press Conference Black Holes and Gamma-Ray Bursts (by Susanna Kohler)The final press conference of the meeting covered three topics from the categories of black holes and gamma-ray bursts.Fred Rasio (CIERA/Northwestern University) opened the conference with a discussion of how the systems that LIGO detected might have formed. There are two primary models for how these black-hole binaries are created. In the first, they start out as binary systems of two massive stars. If the binary survives the process of both stars collapsing into black holes, then a binary black hole system results.Rasio focused on the second theory, in which that black holes are formed in dense stellar clusters. These black holes then sink (via dynamical friction) to the centers of the clusters like dust particles settling on the floor of a room, where they form binaries in a black hole mosh pit eventually getting kicked out of the cluster by dynamical interactions. You can read more about their research in the press release here.Rasio presents a pretty awesome animation of this black hole mosh pit. astrobites (@astrobites) June 15, 2016The effects of a spinning black hole on the spacetime around it. [J.P. Eekels J.M. Overduin]Next up was Richard Henry (Johns Hopkins University), who spoke about the internal structure of spinning black holes (known as Kerr black holes). Because no light can escape from
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Editors Note:This week were at the 227th AAS Meeting in Kissimmee, FL. Along with several fellow authors from astrobites.com, I will bewritingupdates on selectedevents at themeeting and posting at the end of each day. Follow along here or atastrobites.com, or catch ourlive-tweeted updates from the@astrobites Twitter account. The usual posting schedule for AAS Nova will resumenext week.Welcome to Day 3 of the winter American Astronomical Society (AAS) meeting in Kissimmee! Several of us are attending the conference this year, and we will report highlights from each day here on astrobites. If youd like to see more timely updates during the day, we encourage you to follow @astrobites on twitter or search the #aas227 hashtag.Henry Norris Russell Lecture: Viewing the Universe with Infrared Eyes: The Spitzer Space Telescope (by Erika Nesvold)The Henry Norris Russell Award is the highest honor given by the AAS, for a lifetime of eminence in astronomy research. This years award went to Giovanni Fazio of the Harvard-Smithsonian Center for Astrophysics. Fazio became a leader in gamma ray astronomy before switching mid-career to the study of infrared astronomy, and he gave his award lecture on the latter subject, specifically on the Spitzer Space Telescope, one of the most successful infrared telescopes of all time.Artists rendering of the Spitzer space telescope. [NASA/JPL-Caltech]Spitzer has been operating for more than twelve years, and has resulted in over six thousand papers in refereed journals in that time. The telescope sits in an Earth-trailing orbit around the Sun, and is now farther from the Earth (1.4 AU) than the Earth is from the Sun. Fazio gave the audience a fascinating overview of the science done by Spitzer over more than a decade. One of the most productive areas of research for Spitzer is the study of exoplanets, which hadnt even been discovered when the Spitzer Telescope was first conceived. Spitzers high sensitivity and ability to observe exoplanets over
The Akt/mTOR pathway is a key driver of murine CD4 + T cell differentiation, and induction of regulatory T (Treg) cells results from low TCR signal strength and low Akt/mTOR signaling. However, strong TCR signals induce high Akt activity that promotes Th cell induction. Yet, it is unclear how Akt controls alternate T cell fate decisions. We find that the strength of the TCR signal results in differential Akt enzymatic activity. Surprisingly, the Akt substrate networks associated with T cell fate decisions are qualitatively different. Proteomic profiling of Akt signaling networks during Treg versus Th induction demonstrates that Akt differentially regulates RNA processing and splicing factors to drive T cell differentiation. Interestingly, heterogeneous nuclear ribonucleoprotein (hnRNP) L or hnRNP A1 are Akt substrates during Treg induction and have known roles in regulating the stability and splicing of key mRNAs that code for proteins in the canonical TCR signaling pathway, including CD3ζ and CD45. Functionally, inhibition of Akt enzymatic activity results in the dysregulation of splicing during T cell differentiation, and knockdown of hnRNP L or hnRNP A1 results in the lower induction of Treg cells. Together, this work suggests that a switch in substrate specificity coupled to the phosphorylation status of Akt may lead to alternative cell fates and demonstrates that proteins involved with alternative splicing are important factors in T cell fate decisions. Copyright 2017 by The American Association of Immunologists, Inc.
Contact-dependent growth inhibition (CDI) is a mechanism of inter-cellular competition in which Gram-negative bacteria exchange polymorphic toxins using type V secretion systems. Here, we present structures of the CDI toxin from Escherichia coli NC101 in ternary complex with its cognate immunity protein and elongation factor Tu (EF-Tu). The toxin binds exclusively to domain 2 of EF-Tu, partially overlapping the site that interacts with the 3'-end of aminoacyl-tRNA (aa-tRNA). The toxin exerts a unique ribonuclease activity that cleaves the single-stranded 3'-end from tRNAs that contain guanine discriminator nucleotides. EF-Tu is required to support this tRNase activity in vitro, suggesting the toxinmore specifically cleaves substrate in the context of GTPEF-Tuaa-tRNA complexes. However, superimposition of the toxin domain onto previously solved GTPEF-Tuaa-tRNA structures reveals potential steric clashes with both aa-tRNA and the switch I region of EF-Tu. Further, the toxin induces conformational changes in EF-Tu, displacing a β-hairpin loop that forms a critical salt-bridge contact with the 3'-terminal adenylate of aa-tRNA. Altogether, these observations suggest that the toxin remodels GTPEF-Tuaa-tRNA complexes to free the 3'-end of aa-tRNA for entry into the nuclease active site. less
Migration speed and directionality switch of normal epithelial cells after TGF-β1-induced EMT (tEMT) on micro-structured polydimethylsiloxane (PDMS) substrates with variations in stiffness and topographic patterning. 2ff7e9595c
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