Superburst oscillations: ocean and crustal modes excited by Carbon-triggered Type I X-ray bursts

Accreting neutron stars (NS) can exhibit high frequency modulations in their lightcurves during thermonuclear X-ray bursts, known as burst oscillations. The frequencies can be offset from the spin frequency of the NS by several Hz, and can drift by 1-3 Hz. One possible explanation is a mode in the bursting ocean, the frequency of which would decrease (in the rotating frame) as the burst cools, hence explaining the drifts. Most burst oscillations have been observed during H/He triggered bursts, however there has been one observation of oscillations during a superburst; hours' long Type I X-ray bursts caused by unstable carbon burning deeper in the ocean. This paper calculates the frequency evolution of an oceanic r-mode during a superburst. The rotating frame frequency varies during the burst from 4-14 Hz, and is sensitive to the background parameters, in particular the temperature of the ocean and ignition depth. This calculation is compared to the superburst oscillations observed on 4U-1636-536. The predicted mode frequencies ($\sim$ 10 Hz) would require a spin frequency of $\sim$ 592 Hz to match observations; 6 Hz higher than the spin inferred from an oceanic r-mode model for the H/He triggered burst oscillations. This model also over-predicts the frequency drift during the superburst by 90 %.Comment: Accepted for publication in MNRA

A role for chromatin remodellers in replication of damaged DNA

In eukaryotic cells, replication past damaged sites in DNA is regulated by the ubiquitination of proliferating cell nuclear antigen (PCNA). Little is known about how this process is affected by chromatin structure. There are two isoforms of the Remodels the Structure of Chromatin (RSC) remodelling complex in yeast. We show that deletion of RSC2 results in a dramatic reduction in the level of PCNA ubiquitination after DNA-damaging treatments, whereas no such effect was observed after deletion of RSC1. Similarly, depletion of the BAF180 component of the corresponding PBAF (Polybromo BRG1 (Brahma-Related Gene 1) Associated Factor) complex in human cells led to a similar reduction in PCNA ubiquitination. Remarkably, we found that depletion of BAF180 resulted after UV-irradiation, in a reduction not only of ubiquitinated PCNA but also of chromatin-associated unmodified PCNA and Rad18 (the E3 ligase that ubiquitinates PCNA). This was accompanied by a modest decrease in fork progression. We propose a model to account for these findings that postulates an involvement of PBAF in repriming of replication downstream from replication forks blocked at sites of DNA damage. In support of this model, chromatin immunoprecipitation data show that the RSC complex in yeast is present in the vicinity of the replication forks, and by extrapolation, this is also likely to be the case for the PBAF complex in human cells

Fork rotation and DNA precatenation are restricted during DNA replication to prevent chromosomal instability

Faithful genome duplication and inheritance require the complete resolution of all intertwines within the parental DNA duplex. This is achieved by topoisomerase action ahead of the replication fork or by fork rotation and subsequent resolution of the DNA precatenation formed. Although fork rotation predominates at replication termination, in vitro studies have suggested that it also occurs frequently during elongation. However, the factors that influence fork rotation and how rotation and precatenation may influence other replication-associated processes are unknown. Here we analyze the causes and consequences of fork rotation in budding yeast. We find that fork rotation and precatenation preferentially occur in contexts that inhibit topoisomerase action ahead of the fork, including stable protein–DNA fragile sites and termination. However, generally, fork rotation and precatenation are actively inhibited by Timeless/Tof1 and Tipin/Csm3. In the absence of Tof1/Timeless, excessive fork rotation and precatenation cause extensive DNA damage following DNA replication. With Tof1, damage related to precatenation is focused on the fragile protein–DNA sites where fork rotation is induced. We conclude that although fork rotation and precatenation facilitate unwinding in hard-to-replicate contexts, they intrinsically disrupt normal chromosome duplication and are therefore restricted by Timeless/Tipin

Deep model simulation of polar vortices in gas giant atmospheres

The Cassini and Juno probes have revealed large coherent cyclonic vortices in the polar regions of Saturn and Jupiter, a dramatic contrast from the east-west banded jet structure seen at lower latitudes. Debate has centered on whether the jets are shallow, or extend to greater depths in the planetary envelope. Recent experiments and observations have demonstrated the relevance of deep convection models to a successful explanation of jet structure and cyclonic coherent vortices away from the polar regions have been simulated recently including an additional stratified shallow layer. Here we present new convective models able to produce long-lived polar vortices. Using simulation parameters relevant for giant planet atmospheres we find flow regimes that are in agreement with geostrophic turbulence (GT) theory in rotating convection for the formation of large scale coherent structures via an upscale energy transfer fully three-dimensional. Our simulations generate polar characteristics qualitatively similar to those seen by Juno and Cassini: they match the structure of cyclonic vortices seen on Jupiter; or can account for the existence of a strong polar vortex extending downwards to lower latitudes with a marked spiral morphology and the hexagonal pattern seen on Saturn. Our findings indicate that these vortices can be generated deep in the planetary interior. A transition differentiating these two polar flows regimes is described, interpreted in terms of different force balances and compared with previous shallow atmospheric models which characterised polar vortex dynamics in giant planets. In addition, the heat transport properties are investigated confirming recent scaling laws obtained in the context of reduced models of GT.Comment: 18 pages, 13 figures and 3 table

Waves in Thin Oceans on Oblate Neutron Stars

Waves in thin fluid layers are important in various stellar and planetary problems. Due to rapid rotation such systems will become oblate, with a latitudinal variation in the gravitational acceleration across the surface of the object. In the case of accreting neutron stars, rapid rotation could lead to a polar radius smaller than the equatorial radius by a factor $\sim 0.8$. We investigate how the oblateness and a changing gravitational acceleration affect different hydrodynamic modes that exist in such fluid layers through analytic approximations and numerical calculations. The wave vectors of $g$-modes and Yanai modes increase for more oblate systems compared to spherical counterparts, although the impact of variations in the changing gravitational acceleration is effectively negligible. We find that for increased oblateness, Kelvin modes show less equatorial confinement and little change in their wave vector. For $r$-modes, we find that for more oblate systems the wave vector decreases. The exact manner of these changes for the $r$-modes depends on the model for the gravitational acceleration across the surface.Comment: 10 pages, 8 figures Accepted for publication in MNRA

BAF180 promotes cohesion and prevents genome instability and aneuploidy

BAF180, a subunit of the PBAF chromatin remodeling complex, is frequently mutated in cancer. Although PBAF regulates transcription, it remains unclear whether this is what drives tumorigenesis in cells lacking BAF180. Based on data from yeast, we hypothesized that BAF180 may prevent tumorigenesis by promoting cohesion. Here, we show BAF180 is required for centromeric cohesion in mouse and human cells. Mutations identified in tumor samples are unable to support this activity, and also compromise cohesion-dependent functions in yeast. We provide evidence of genome instability in line with loss of cohesion, and importantly, we find dynamic chromosome instability following DNA damage in cells lacking BAF180. These data demonstrate a function for BAF180 in promoting genome stability that is distinct from its well-characterized role in transcriptional regulation, uncovering a potent mechanism for its tumor-suppressor activity

Requirement for PBAF in transcriptional repression and repair at DNA breaks in actively transcribed regions of chromatin

Actively transcribed regions of the genome are vulnerable to genomic instability. Recently, it was discovered that transcription is repressed in response to neighboring DNA double-strand breaks (DSBs). It is not known whether a failure to silence transcription flanking DSBs has any impact on DNA repair efficiency or whether chromatin remodelers contribute to the process. Here, we show that the PBAF remodeling complex is important for DSB-induced transcriptional silencing and promotes repair of a subset of DNA DSBs at early time points, which can be rescued by inhibiting transcription globally. An ATM phosphorylation site on BAF180, a PBAF subunit, is required for both processes. Furthermore, we find that subunits of the PRC1 and PRC2 polycomb group complexes are similarly required for DSB-induced silencing and promoting repair. Cancer-associated BAF180 mutants are unable to restore these functions, suggesting PBAF's role in repressing transcription near DSBs may contribute to its tumor suppressor activity

The BAH domain of Rsc2 is a histone H3 binding domain

Bromo-adjacent homology (BAH) domains are commonly found in chromatin-associated proteins and fall into two classes; Remodels the Structure of Chromatin (RSC)-like or Sir3-like. Although Sir3-like BAH domains bind nucleosomes, the binding partners of RSC-like BAH domains are currently unknown. The Rsc2 subunit of the RSC chromatin remodeling complex contains an RSC-like BAH domain and, like the Sir3-like BAH domains, we find Rsc2 BAH also interacts with nucleosomes. However, unlike Sir3-like BAH domains, we find that Rsc2 BAH can bind to recombinant purified H3 in vitro, suggesting that the mechanism of nucleosome binding is not conserved. To gain insight into the Rsc2 BAH domain, we determined its crystal structure at 2.4 Å resolution. We find that it differs substantially from Sir3-like BAH domains and lacks the motifs in these domains known to be critical for making contacts with histones. We then go on to identify a novel motif in Rsc2 BAH that is critical for efficient H3 binding in vitro and show that mutation of this motif results in defective Rsc2 function in vivo. Moreover, we find this interaction is conserved across Rsc2-related proteins. These data uncover a binding target of the Rsc2 family of BAH domains and identify a novel motif that mediates this interaction