Nucleotide excision repair II: From yeast to mammals

An intricate network of repair systems safeguards the integrity of genetic material, by eliminating DNA lesions induced by numerous environmental and endogenous genotoxic agents. Nucleotide excision repair (NER) is one of the most versatile DNA repair systems. Deficiencies in this process give rise to the classical human DNA repair disorders xeroderma pigmentosum (XP) and Cockayne's syndrome (CS), and to a recently recognized disease called PIBIDS, a photosensitive form of the brittle hair disorder trichothiodystrophy. This is the second of a two-part review on NER. Part I (in the previous issue of TIG) concentrated on the main characteristics of the NER pathway of E. coli and yeast. Part II compares the mammalian and yeast systems, and attempts to integrate current knowledge on the eukaryotic pathway to suggest an outline for the reaction mechanism

Incisions for excision

Excison implies two incisions. Plumbers and surgeons know this principle, and long ago it was put into practice by the evolutionarily ancient DNA-repair machinery. Dissection of the first incision made by the eukaryotic nucleotide-excision repair pathway has now been described by O'Donovan et al., and dissection of the second by Bardwell et al. When put together the two processes enable the replacement of a damaged piece of DNA by a new one. [...]One might predict that a category of patients will be found that are deficient in nucleotide-excision repair and also have symptoms of a recombination defect. If these striking multiple engagements reflect a general evolutionary strategy of function sharing, then intimate connections between nucleotide-excision repair and cell-cycle control or chromatin dynamics are bound to show up as well

Incisions for excision

Excison implies two incisions. Plumbers and surgeons know this principle, and long ago it was put into practice by the evolutionarily ancient DNA-repair machinery. Dissection of the first incision made by the eukaryotic nucleotide-excision repair pathway has now been described by O'Donovan et al., and dissection of the second by Bardwell et al. When put together the two processes enable the replacement of a damaged piece of DNA by a new one. [...]One might predict that a category of patients will be found that are deficient in nucleotide-excision repair and also have symptoms of a recombination defect. If these striking multiple engagements reflect a general evolutionary strategy of function sharing, then intimate connections between nucleotide-excision repair and cell-cycle control or chromatin dynamics are bound to show up as well

Phase diagram of orbital-selective Mott transitions at finite temperatures

Mott transitions in the two-orbital Hubbard model with different bandwidths are investigated at finite temperatures. By means of the self-energy functional approach, we discuss the stability of the intermediate phase with one orbital localized and the other itinerant, which is caused by the orbital-selective Mott transition (OSMT). It is shown that the OSMT realizes two different coexistence regions at finite temperatures in accordance with the recent results of Liebsch. We further find that the particularly interesting behavior emerges around the special condition $U=U'$ and J=0, which includes a new type of the coexistence region with three distinct states. By systematically changing the Hund coupling, we establish the global phase diagram to elucidate the key role played by the Hund coupling on the Mott transitions.Comment: 4 pages, 6 figure

On General Axial Gauges for QCD

General Axial Gauges within a perturbative approach to QCD are plagued by 'spurious' propagator singularities. Their regularisation has to face major conceptual and technical problems. We show that this obstacle is naturally absent within a Wilsonian or 'Exact' Renormalisation Group approach and explain why this is so. The axial gauge turns out to be a fixed point under the flow, and the universal 1-loop running of the gauge coupling is computed.Comment: 4 pages, latex, talk presented by DFL at QCD'98, Montpellier, July 2-8, 1998; to be published in Nucl. Phys. B (Proc. Suppl.

Nucleotide excision repair I: from E.coli to yeast.

Genetic information is constantly deteriorating, mainly as a consequence of the action of numerous genotoxic agents. In order to cope with this fundamental problem, all living organisms have acquired a complex network of DNA repair systems to safeguard their genetic integrity. Nucleotide excision repair (NER), one of the most important of these, is a complex multi-enzyme reaction that removes a remarkably wide range of lesions. This is the first of a series of two reviews on this repair process. Part I focuses on the main characteristics of the NER pathway in E. coli and yeast. Part II, to appear in the next issue of TIG, deals with NER in mammals and compares it with the process in yeast