RAD6-RAD18-RAD5-pathway-dependent tolerance to chronic low-dose ultraviolet light

In nature, organisms are exposed to chronic low- dose ultraviolet light ( CLUV) as opposed to the acute high doses common to laboratory experiments. Analysis of the cellular response to acute high-dose exposure has delineated the importance of direct DNA repair by the nucleotide excision repair pathway(1) and for checkpoint-induced cell cycle arrest in promoting cell survival(2). Here we examine the response of yeast cells to CLUV and identify a key role for the RAD6-RAD18-RAD5 error- free postreplication repair (RAD6 error-free PRR) pathway(3,4) in promoting cell growth and survival. We show that loss of the RAD6 error- free PRR pathway results in DNA-damage-checkpoint- induced G2 arrest in CLUV-exposed cells, whereas wild-type and nucleotide-excision-repair-deficient cells are largely unaffected. Cell cycle arrest in the absence of the RAD6 error- free PRR pathway was not caused by a repair defect or by the accumulation of ultraviolet-induced photoproducts. Notably, we observed increased replication protein A (RPA) and Rad52 - yellow fluorescent protein foci(5) in the CLUV- exposed rad18 Delta cells and demonstrated that Rad52- mediated homologous recombination is required for the viability of the rad18 Delta cells after release from CLUV- induced G2 arrest. These and other data presented suggest that, in response to environmental levels of ultraviolet exposure, the RAD6 error- free PRR pathway promotes replication of damaged templates without the generation of extensive single- stranded DNA regions. Thus, the error- free PRR pathway is specifically important during chronic low- dose ultraviolet exposure to prevent counter- productive DNA checkpoint activation and allow cells to proliferate normally

Unbinding Transition Induced by Osmotic Pressure in Relation to Unilamellar Vesicle Formation

Small-angle X-ray scattering and phase-contrast microscopy experiments were performed to investigate the effect of the osmotic pressure on vesicle formation in a dioleoylphosphatidylcholine (DOPC)/water/NaI system. Multi-lamellar vesicles were formed when a pure lipid film was hydrated with an aqueous solution of NaI. On the other hand, uni-lamellar vesicles (ULVs) were formed when a lipid film mixed with an enough amount of NaI was hydrated. To confirm the effect of the osmotic pressure due to NaI, a free-energy calculation was performed. This result showed that the osmotic pressure induced an unbinding transition on the hydration process, which resulted in ULV formation

Well-posedness of the Viscous Boussinesq System in Besov Spaces of Negative Order Near Index s=−1s=-1

This paper is concerned with well-posedness of the Boussinesq system. We prove that the $n$ ($n\ge2$) dimensional Boussinesq system is well-psoed for small initial data $(\vec{u}_0,\theta_0)$ ($\nabla\cdot\vec{u}_0=0$) either in $({B}^{-1}_{\infty,1}\cap{B^{-1,1}_{\infty,\infty}})\times{B}^{-1}_{p,r}$ or in ${B^{-1,1}_{\infty,\infty}}\times{B}^{-1,\epsilon}_{p,\infty}$ if $r\in[1,\infty]$, $\epsilon>0$ and $p\in(\frac{n}{2},\infty)$, where $B^{s,\epsilon}_{p,q}$ ($s\in\mathbb{R}$, $1\leq p,q\leq\infty$, $\epsilon>0$) is the logarithmically modified Besov space to the standard Besov space $B^{s}_{p,q}$. We also prove that this system is well-posed for small initial data in $({B}^{-1}_{\infty,1}\cap{B^{-1,1}_{\infty,\infty}})\times({B}^{-1}_{\frac{n}{2},1}\cap{B^{-1,1}_{\frac{n}{2},\infty}})$.Comment: 18 page

On the Navier-Stokes equations with rotating effect and prescribed outflow velocity

We consider the equations of Navier-Stokes modeling viscous fluid flow past a moving or rotating obstacle in $\mathbb{R}^d$ subject to a prescribed velocity condition at infinity. In contrast to previously known results, where the prescribed velocity vector is assumed to be parallel to the axis of rotation, in this paper we are interested in a general outflow velocity. In order to use $L^p$-techniques we introduce a new coordinate system, in which we obtain a non-autonomous partial differential equation with an unbounded drift term. We prove that the linearized problem in $\mathbb{R}^d$ is solved by an evolution system on $L^p_{\sigma}(\mathbb{R}^d)$ for $1<p<\infty$. For this we use results about time-dependent Ornstein-Uhlenbeck operators. Finally, we prove, for $p\geq d$ and initial data $u_0\in L^p_{\sigma}(\mathbb{R}^d)$, the existence of a unique mild solution to the full Navier-Stokes system.Comment: 18 pages, to appear in J. Math. Fluid Mech. (published online first

ruvA Mutants that resolve Holliday junctions but do not reverse replication forks

RuvAB and RuvABC complexes catalyze branch migration and resolution of Holliday junctions (HJs) respectively. In addition to their action in the last steps of homologous recombination, they process HJs made by replication fork reversal, a reaction which occurs at inactivated replication forks by the annealing of blocked leading and lagging strand ends. RuvAB was recently proposed to bind replication forks and directly catalyze their conversion into HJs. We report here the isolation and characterization of two separation-of-function ruvA mutants that resolve HJs, based on their capacity to promote conjugational recombination and recombinational repair of UV and mitomycin C lesions, but have lost the capacity to reverse forks. In vivo and in vitro evidence indicate that the ruvA mutations affect DNA binding and the stimulation of RuvB helicase activity. This work shows that RuvA's actions at forks and at HJs can be genetically separated, and that RuvA mutants compromised for fork reversal remain fully capable of homologous recombination