336 research outputs found
Characterization of a Y-Family DNA Polymerase eta from the Eukaryotic Thermophile Alvinella pompejana
Human DNA polymerase η (HsPolη) plays an important role in translesion synthesis (TLS), which allows for replication past DNA damage such as UV-induced cis-syn cyclobutane pyrimidine dimers (CPDs). Here, we characterized ApPolη from the thermophilic worm Alvinella pompejana, which inhabits deep-sea hydrothermal vent chimneys. ApPolη shares sequence homology with HsPolη and contains domains for binding ubiquitin and proliferating cell nuclear antigen. Sun-induced UV does not penetrate Alvinella's environment; however, this novel DNA polymerase catalyzed efficient and accurate TLS past CPD, as well as 7,8-dihydro-8-oxoguanine and isomers of thymine glycol induced by reactive oxygen species. In addition, we found that ApPolη is more thermostable than HsPolη, as expected from its habitat temperature. Moreover, the activity of this enzyme was retained in the presence of a higher concentration of organic solvents. Therefore, ApPolη provides a robust, human-like Polη that is more active after exposure to high temperatures and organic solvents
Marginalization of end-use technologies in energy innovation for climate protection
Mitigating climate change requires directed innovation efforts to develop and deploy energy technologies. Innovation activities are directed towards the outcome of climate protection by public institutions, policies and resources that in turn shape market behaviour. We analyse diverse indicators of activity throughout the innovation system to assess these efforts. We find efficient end-use technologies contribute large potential emission reductions and provide higher social returns on investment than energy-supply technologies. Yet public institutions, policies and financial resources pervasively privilege energy-supply technologies. Directed innovation efforts are strikingly misaligned with the needs of an emissions-constrained world. Significantly greater effort is needed to develop the full potential of efficient end-use technologies
Plasmoid-Induced-Reconnection and Fractal Reconnection
As a key to undertanding the basic mechanism for fast reconnection in solar
flares, plasmoid-induced-reconnection and fractal reconnection are proposed and
examined. We first briefly summarize recent solar observations that give us
hints on the role of plasmoid (flux rope) ejections in flare energy release. We
then discuss the plasmoid-induced-reconnection model, which is an extention of
the classical two-ribbon-flare model which we refer to as the CSHKP model. An
essential ingredient of the new model is the formation and ejection of a
plasmoid which play an essential role in the storage of magnetic energy (by
inhibiting reconnection) and the induction of a strong inflow into reconnection
region. Using a simple analytical model, we show that the plasmoid ejection and
acceleration are closely coupled with the reconnection process, leading to a
nonlinear instability for the whole dynamics that determines the macroscopic
reconnection rate uniquely. Next we show that the current sheet tends to have a
fractal structure via the following process path: tearing, sheet thinning,
Sweet- Parker sheet, secondary tearing, further sheet thinning... These
processes occur repeatedly at smaller scales until a microscopic plasma scale
(either the ion Larmor radius or the ion inertial length) is reached where
anomalous resistivity or collisionless reconnection can occur. The current
sheet eventually has a fractal structure with many plasmoids (magnetic islands)
of different sizes. When these plasmoids are ejected out of the current sheets,
fast reconnection occurs at various different scales in a highly time dependent
manner. Finally, a scenario is presented for fast reconnection in the solar
corona on the basis of above plasmoid-induced-reconnection in a fractal current
sheet.Comment: 9 pages, 11 figures, with using eps.sty; Earth, Planets and Space in
press; ps-file is also available at
http://stesun8.stelab.nagoya-u.ac.jp/~tanuma/study/shibata2001
Simultaneous disruption of two DNA polymerases, Polη and Polζ, in Avian DT40 cells unmasks the role of Polη in cellular response to various DNA lesions
Replicative DNA polymerases are frequently stalled by DNA lesions. The resulting replication blockage is released by homologous recombination (HR) and translesion DNA synthesis (TLS). TLS employs specialized TLS polymerases to bypass DNA lesions. We provide striking in vivo evidence of the cooperation between DNA polymerase η, which is mutated in the variant form of the cancer predisposition disorder xeroderma pigmentosum (XP-V), and DNA polymerase ζ by generating POLη−/−/POLζ−/− cells from the chicken DT40 cell line. POLζ−/− cells are hypersensitive to a very wide range of DNA damaging agents, whereas XP-V cells exhibit moderate sensitivity to ultraviolet light (UV) only in the presence of caffeine treatment and exhibit no significant sensitivity to any other damaging agents. It is therefore widely believed that Polη plays a very specific role in cellular tolerance to UV-induced DNA damage. The evidence we present challenges this assumption. The phenotypic analysis of POLη−/−/POLζ−/− cells shows that, unexpectedly, the loss of Polη significantly rescued all mutant phenotypes of POLζ−/− cells and results in the restoration of the DNA damage tolerance by a backup pathway including HR. Taken together, Polη contributes to a much wide range of TLS events than had been predicted by the phenotype of XP-V cells
Identification of genes potentially involved in supporting hematopoietic stem cell activity of stromal cell line MC3T3-G2/PA6
Although coculture of hematopoietic stem cells (HSCs) with stromal cells is a useful system to study hematopoiesis in the niche, little is known regarding the precise cellular and molecular mechanisms of maintaining HSCs through cell–cell interactions. The murine preadipose stromal cell line MC3T3-G2/PA6 (PA6) has been demonstrated to support HSCs in vitro. In this study, microarray analysis was performed on PA6 cells and HSC-nonsupporting PA6 subclone cells to identify genes responsible for supporting HSC activity. Comparison of gene expression profiles revealed that only 144 genes were down-regulated by more than twofold in PA6 subclone cells. Of these down-regulated genes, we selected 11 candidate genes and evaluated for the maintenance of HSC function by overexpressing these genes in PA6 subclone cells. One unknown gene, 1110007F12Rik (also named as Tmem140), which is predicted to encode an integral membrane protein, demonstrated a partial restoration of the defect in HSC-supporting activity
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