The kinematics of ionized gas in lyman-break analogs at z ~ 0.2

We present results for 19 “Lyman-break analogs” observed with Keck/OSIRIS with an adaptive-optics-assisted spatial resolution of less than 200 pc. We detect satellites/companions, diffuse emission, and velocity shear, all with high signal-to-noise ratios. These galaxies present remarkably high velocity dispersion along the line of sight (~70 km s^(−1)), much higher than standard star-forming spirals in the low-redshift universe. We artificially redshift our data to z ~ 2.2 to allow for a direct comparison with observations of high-z Lyman-break galaxies and find striking similarities between both samples. This suggests that either similar physical processes are responsible for their observed properties, or, alternatively, that it is very difficult to distinguish between different mechanisms operating in the low- versus high-redshift starburst galaxies based on the available data. The comparison between morphologies in the UV/optical continuum and our kinemetry analysis often shows that neither is by itself sufficient to confirm or completely rule out the contribution from recent merger events. We find a correlation between the kinematic properties and stellar mass, in that more massive galaxies show stronger evidence for a disk-like structure. This suggests a co-evolutionary process between the stellar mass buildup and the formation of morphological and dynamical substructure within the galaxy

A tri-ionic anchor mechanism drives Ube2N-specific recruitment and K63-chain ubiquitination in TRIM ligases.

The cytosolic antibody receptor TRIM21 possesses unique ubiquitination activity that drives broad-spectrum anti-pathogen targeting and underpins the protein depletion technology Trim-Away. This activity is dependent on formation of self-anchored, K63-linked ubiquitin chains by the heterodimeric E2 enzyme Ube2N/Ube2V2. Here we reveal how TRIM21 facilitates ubiquitin transfer and differentiates this E2 from other closely related enzymes. A tri-ionic motif provides optimally distributed anchor points that allow TRIM21 to wrap an Ube2N~Ub complex around its RING domain, locking the closed conformation and promoting ubiquitin discharge. Mutation of these anchor points inhibits ubiquitination with Ube2N/Ube2V2, viral neutralization and immune signalling. We show that the same mechanism is employed by the anti-HIV restriction factor TRIM5 and identify spatially conserved ionic anchor points in other Ube2N-recruiting RING E3s. The tri-ionic motif is exclusively required for Ube2N but not Ube2D1 activity and provides a generic E2-specific catalysis mechanism for RING E3s

Nitrogen Production in Starburst Galaxies Detected by GALEX

We investigate the production of nitrogen in star-forming galaxies with ultraviolet (UV) radiation detected by the Galaxy Evolution Explorer Satellite (GALEX). We use a sample of 8745 GALEX emission-line galaxies matched to the Sloan Digital Sky Survey (SDSS) spectroscopic sample. We derive both gas-phase oxygen and nitrogen abundances for the sample and apply stellar population synthesis models to derive stellar masses and star formation histories of the galaxies. We compare oxygen abundances derived using three different diagnostics. We derive the specific star formation rates of the galaxies by modeling the seven-band GALEX+SDSS photometry. We find that galaxies that have log (SFR/M_*) ≳ − 10.0 typically have values of log (N/O) ~ 0.05 dex less than galaxies with log (SFR/M_*) ≾ − 10.0 and similar oxygen abundances

Furin cleavage of SARS-CoV-2 Spike promotes but is not essential for infection and cell-cell fusion.

Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infects cells by binding to the host cell receptor ACE2 and undergoing virus-host membrane fusion. Fusion is triggered by the protease TMPRSS2, which processes the viral Spike (S) protein to reveal the fusion peptide. SARS-CoV-2 has evolved a multibasic site at the S1-S2 boundary, which is thought to be cleaved by furin in order to prime S protein for TMPRSS2 processing. Here we show that CRISPR-Cas9 knockout of furin reduces, but does not prevent, the production of infectious SARS-CoV-2 virus. Comparing S processing in furin knockout cells to multibasic site mutants reveals that while loss of furin substantially reduces S1-S2 cleavage it does not prevent it. SARS-CoV-2 S protein also mediates cell-cell fusion, potentially allowing virus to spread virion-independently. We show that loss of furin in either donor or acceptor cells reduces, but does not prevent, TMPRSS2-dependent cell-cell fusion, unlike mutation of the multibasic site that completely prevents syncytia formation. Our results show that while furin promotes both SARS-CoV-2 infectivity and cell-cell spread it is not essential, suggesting furin inhibitors may reduce but not abolish viral spread

IP6 is an HIV pocket factor that prevents capsid collapse and promotes DNA synthesis.

The HIV capsid is semipermeable and covered in electropositive pores that are essential for viral DNA synthesis and infection. Here, we show that these pores bind the abundant cellular polyanion IP6, transforming viral stability from minutes to hours and allowing newly synthesised DNA to accumulate inside the capsid. An arginine ring within the pore coordinates IP6, which strengthens capsid hexamers by almost 10°C. Single molecule measurements demonstrate that this renders native HIV capsids highly stable and protected from spontaneous collapse. Moreover, encapsidated reverse transcription assays reveal that, once stabilised by IP6, the accumulation of new viral DNA inside the capsid increases >100 fold. Remarkably, isotopic labelling of inositol in virus-producing cells reveals that HIV selectively packages over 300 IP6 molecules per infectious virion. We propose that HIV recruits IP6 to regulate capsid stability and uncoating, analogous to picornavirus pocket factors. HIV-1/IP6/capsid/co-factor/reverse transcription

Furin cleavage of SARS-CoV-2 Spike promotes but is not essential for infection and cell-cell fusion.

Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) infects cells by binding to the host cell receptor ACE2 and undergoing virus-host membrane fusion. Fusion is triggered by the protease TMPRSS2, which processes the viral Spike (S) protein to reveal the fusion peptide. SARS-CoV-2 has evolved a multibasic site at the S1-S2 boundary, which is thought to be cleaved by furin in order to prime S protein for TMPRSS2 processing. Here we show that CRISPR-Cas9 knockout of furin reduces, but does not prevent, the production of infectious SARS-CoV-2 virus. Comparing S processing in furin knockout cells to multibasic site mutants reveals that while loss of furin substantially reduces S1-S2 cleavage it does not prevent it. SARS-CoV-2 S protein also mediates cell-cell fusion, potentially allowing virus to spread virion-independently. We show that loss of furin in either donor or acceptor cells reduces, but does not prevent, TMPRSS2-dependent cell-cell fusion, unlike mutation of the multibasic site that completely prevents syncytia formation. Our results show that while furin promotes both SARS-CoV-2 infectivity and cell-cell spread it is not essential, suggesting furin inhibitors may reduce but not abolish viral spread

UV Star Formation Rates in the Local Universe

We measure star formation rates of ~50,000 optically-selected galaxies in the local universe (z~0.1), spanning a range from gas-rich dwarfs to massive ellipticals. We obtain dust-corrected SFRs by fitting the GALEX (UV) and SDSS (optical) photometry to a library of population synthesis models that include dust attenuation. For star-forming galaxies, our UV-based SFRs compare remarkably well with those derived from SDSS H alpha. Deviations from perfect agreement between these two methods are due to differences in the dust attenuation estimates. In contrast to H alpha, UV provides reliable SFRs for galaxies with weak or no H alpha emission, and where H alpha is contaminated with an emission from an AGN. We use full-SED SFRs to calibrate a simple prescription that uses GALEX UV magnitudes to produce good SFRs for normal star-forming galaxies. The specific SFR is considered as a function of stellar mass for (1) star-forming galaxies with no AGN, (2) those hosting an AGN, and for (3) galaxies without H alpha emission. We find that the three have distinct star formation histories, with AGN lying intermediate between the star-forming and the quiescent galaxies. Normal star forming galaxies (without an AGN) lie on a relatively narrow linear sequence. Remarkably, galaxies hosting a strong AGN appear to represent the massive continuation of this sequence. Weak AGN, while also massive, have lower SFR, sometimes extending to the realm of quiescent galaxies. We propose an evolutionary sequence for massive galaxies that smoothly connects normal star-forming galaxies to quiescent (red sequence) galaxies via strong and weak AGN. We confirm that some galaxies with no H alpha emission show signs of SF in the UV. We derive a UV-based cosmic SFR density at z=0.1 with smaller total error than previous measurements (abridged).Comment: Accepted for publication in ApJ (Special GALEX Supplement issue - Dec 2007). v2: Typo in Eq. 2 correcte

A lysine ring in HIV capsid pores coordinates IP6 to drive mature capsid assembly.

The HIV capsid self-assembles a protective conical shell that simultaneously prevents host sensing whilst permitting the import of nucleotides to drive DNA synthesis. This is accomplished through the construction of dynamic, highly charged pores at the centre of each capsid multimer. The clustering of charges required for dNTP import is strongly destabilising and it is proposed that HIV uses the metabolite IP6 to coordinate the pore during assembly. Here we have investigated the role of inositol phosphates in coordinating a ring of positively charged lysine residues (K25) that forms at the base of the capsid pore. We show that whilst IP5, which can functionally replace IP6, engages an arginine ring (R18) at the top of the pore, the lysine ring simultaneously binds a second IP5 molecule. Dose dependent removal of K25 from the pore severely inhibits HIV infection and concomitantly prevents DNA synthesis. Cryo-tomography reveals that K25A virions have a severe assembly defect that inhibits the formation of mature capsid cones. Monitoring both the kinetics and morphology of capsids assembled in vitro reveals that while mutation K25A can still form tubes, the ability of IP6 to drive assembly of capsid cones has been lost. Finally, in single molecule TIRF microscopy experiments, capsid lattices in permeabilised K25 mutant virions are rapidly lost and cannot be stabilised by IP6. These results suggest that the coordination of IP6 by a second charged ring in mature hexamers drives the assembly of conical capsids capable of reverse transcription and infection

PenQuest Volume 2, Number 1

Table of Contents for this Volume: Untitled by Janet Collins Untitled by Judy Gozdur Last Hour of Light by Susan Reed Untitled by Judy Godzur Untitled by Rick Wagner Untitled by Carol Groover Untitled by R. Wagner Only in the Portico by Linda Banicki Untitled by Helen Hagadorn Private Place, Pubic Place by David Reed Untitled by Tammy Hutchinson Untitled by Tammy Hutchinson Madison Knights by Susan Reed Untitled by Sissy Crabtree The Price by Sandra Coleman Untitled by Ann Harrington Invasion of Privacy by Mark Touchton Untitled by Bruce Warner Untitled by Tom Schifanella Untitled by Tammy Hutchinson Bloodwork by Laura Jo Last Untitled by David Whitsett Burial Instructions by Bill Slaughter Untitled by S. Trevett PenQuest Interview: Joe Haldeman by David Reed Her Name Came from the Sea by Richard L. Ewart Untitled by V. Williams In the Woodshed by R. E. Mallery Untitled by Modesta Matthews Untitled by David Olson Illumination by E. Allen Tilley Untitled by Joseph Avanzini Everywoman by Laura Jo Last Untitled by Beth Goeckel Believe Me by Donna Kaluzniak Untitled by Judy Gozdur Untitled by Judy Gozdur Unicorn by David Reed Untitled by Susan Reed untitled by Paul Cramer Unititled by Lucinda Halsema The Violin by Richard L. Ewart Untitled by Maria Barry Untitled by Roger Whitt Jr. Haiku by Lori Nasrallah Rhymer’s Revolt by R. E. Mallery Untitled by Valerie William

The UV-Optical Color Dependence of Galaxy Clustering in the Local Universe

We measure the UV-optical color dependence of galaxy clustering in the local universe. Using the clean separation of the red and blue sequences made possible by the NUV - r color-magnitude diagram, we segregate the galaxies into red, blue and intermediate "green" classes. We explore the clustering as a function of this segregation by removing the dependence on luminosity and by excluding edge-on galaxies as a means of a non-model dependent veto of highly extincted galaxies. We find that \xi (r_p, \pi) for both red and green galaxies shows strong redshift space distortion on small scales -- the "finger-of-God" effect, with green galaxies having a lower amplitude than is seen for the red sequence, and the blue sequence showing almost no distortion. On large scales, \xi (r_p, \pi) for all three samples show the effect of large-scale streaming from coherent infall. On scales 1 Mpc/h < r_p < 10 Mpc/h, the projected auto-correlation function w_p(r_p) for red and green galaxies fits a power-law with slope \gamma ~ 1.93 and amplitude r_0 ~ 7.5 and 5.3, compared with \gamma ~ 1.75 and r_0 ~ 3.9 Mpc/h for blue sequence galaxies. Compared to the clustering of a fiducial L* galaxy, the red, green, and blue have a relative bias of 1.5, 1.1, and 0.9 respectively. The w_p(r_p) for blue galaxies display an increase in convexity at ~ 1 Mpc/h, with an excess of large scale clustering. Our results suggest that the majority of blue galaxies are likely central galaxies in less massive halos, while red and green galaxies have larger satellite fractions, and preferentially reside in virialized structures. If blue sequence galaxies migrate to the red sequence via processes like mergers or quenching that take them through the green valley, such a transformation may be accompanied by a change in environment in addition to any change in luminosity and color.Comment: accepted by MNRA