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101.
Mitochondrial control-region sequences in two shorebird species, the turnstone and the dunlin, and their utility in population genetic studies 总被引:12,自引:0,他引:12
We determined the mitochondrial control-region sequences of five turnstones
(Arenaria interpres) and three dunlins (Calidris alpina). Comparisons
revealed that the central part (part II) is conserved relative to much more
variable parts at the beginning (part I) and the end (part III). This
pattern of sequence conservation is also found in the control regions of
other vertebrates. The average sequence divergence between turnstone and
dunlin was 21.8% for part I, 7.5% for part II, and 29.5% for part III.
Within-species sequence divergence over the entire control region was much
lower, at 0.9% for turnstones and 2.0% for dunlins. In both shorebird
species, part III contains a repetitive sequence composed only of A and C
nucleotides, which has not been found in the control regions of other
birds. A survey of the part I sequences of 25 turnstones and 25 dunlins
sampled around the world revealed that these species have very different
population genetic structures. Dunlins are not only much more
differentiated in their sequences but also have a strongly subdivided
population genetic structure. Pleistocene vicariant events combined with
strong natal philopatry and high mutation rates of the sequences are likely
responsible for this population genetic subdivision. Conversely, part I
sequences of turnstones are weakly differentiated and are geographically
unstructured. We argue that this is not the result of global gene flow but
that, instead turnstones have recently expanded from a refugial population
that was bottlenecked.
相似文献
102.
Substrate specificity of ultraviolet DNA endonuclease (UVDE/Uve1p) from Schizosaccharomyces pombe.
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A M Avery B Kaur J S Taylor J A Mello J M Essigmann P W Doetsch 《Nucleic acids research》1999,27(11):2256-2264
Schizosaccharomyces pombe ultraviolet DNA endonuclease (UVDE or Uve1p) has been shown to cleave 5' to UV light-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts (6-4PP). This endonuclease is believed to function in the initial step in an alternative excision repair pathway for the removal of DNA damage caused by exposure to UV light. An active truncated form of this protein, Delta228-Uve1p, has been successfully overexpressed, affinity purified and partially characterized. In the present study we present data from a detailed substrate specificity trial. We have determined that the substrate range of Uve1p is much greater than was originally believed. We demonstrate that this DNA damage repair protein is capable of recognizing an array of UV-induced DNA photoproducts (cis-syn-, trans-syn I- and trans-syn II CPDs, 6-4PP and Dewar isomers) that cause varying degrees of distortion in a duplex DNA molecule. We also demonstrate that Uve1p recognizes non-UV-induced DNA damage, such as platinum-DNA GG diadducts, uracil, dihydrouracil and abasic sites. This is the first time that a single DNA repair endonuclease with the ability to recognize such a diverse range of lesions has been described. This study suggests that Uve1p and the alternative excision repair pathway may participate broadly in the repair of DNA damage. 相似文献
103.
Klungland A Höss M Gunz D Constantinou A Clarkson SG Doetsch PW Bolton PH Wood RD Lindahl T 《Molecular cell》1999,3(1):33-42
Oxidized pyrimidines in DNA are removed by a distinct base excision repair pathway initiated by the DNA glycosylase--AP lyase hNth1 in human cells. We have reconstituted this single-residue replacement pathway with recombinant proteins, including the AP endonuclease HAP1/APE, DNA polymerase beta, and DNA ligase III-XRCC1 heterodimer. With these proteins, the nucleotide excision repair enzyme XPG serves as a cofactor for the efficient function of hNth1. XPG protein promotes binding of hNth1 to damaged DNA. The stimulation of hNth1 activity is retained in XPG catalytic site mutants inactive in nucleotide excision repair. The data support the model that development of Cockayne syndrome in XP-G patients is related to inefficient excision of endogenous oxidative DNA damage. 相似文献
104.
Natalya P. Degtyareva Lanier Heyburn Joan Sterling Michael A. Resnick Dmitry A. Gordenin Paul W. Doetsch 《Nucleic acids research》2013,41(19):8995-9005
Localized hyper-mutability caused by accumulation of lesions in persistent single-stranded (ss) DNA has been recently found in several types of cancers. An increase in endogenous levels of reactive oxygen species (ROS) is considered to be one of the hallmarks of cancers. Employing a yeast model system, we addressed the role of oxidative stress as a potential source of hyper-mutability in ssDNA by modulation of the endogenous ROS levels and by exposing cells to oxidative DNA-damaging agents. We report here that under oxidative stress conditions the majority of base substitution mutations in ssDNA are caused by erroneous, DNA polymerase (Pol) zeta-independent bypass of cytosines, resulting in C to T transitions. For all other DNA bases Pol zeta is essential for ROS-induced mutagenesis. The density of ROS-induced mutations in ssDNA is lower, compared to that caused by UV and MMS, which suggests that ssDNA could be actively protected from oxidative damage. These findings have important implications for understanding mechanisms of oxidative mutagenesis, and could be applied to development of anticancer therapies and cancer prevention. 相似文献
105.
106.
Studies on the enzymology of apurinic/apyrimidinic (AP) endonucleases from procaryotic and eucaryotic organisms are reviewed. Emphasis will be placed on the enzymes from Escherichia coli from which a considerable portion of our knowledge has been derived. Recent studies on similar enzymes from eucaryotes will be discussed as well. In addition, we will discuss the chemical and physical properties of AP sites and review studies on peptides and acridine derivatives which incise DNA at AP sites. 相似文献
107.
108.
We report the functional and temporal relationship between cellular phenotypes such as oxidative stress, p38MAPK-dependent responses and genomic instability persisting in the progeny of cells exposed to sparsely ionizing low-Linear Energy Transfer (LET) radiation such as X-rays or high-charge and high-energy (HZE) particle high-LET radiation such as 56Fe ions. We found that exposure to low and high-LET radiation increased reactive oxygen species (ROS) levels as a threshold-like response induced independently of radiation quality and dose. This response was sustained for two weeks, which is the period of time when genomic instability is evidenced by increased micronucleus formation frequency and DNA damage associated foci. Indicators for another persisting response sharing phenotypes with stress-induced senescence, including beta galactosidase induction, increased nuclear size, p38MAPK activation and IL-8 production, were induced in the absence of cell proliferation arrest during the first, but not the second week following exposure to high-LET radiation. This response was driven by a p38MAPK-dependent mechanism and was affected by radiation quality and dose. This stress response and elevation of ROS affected genomic instability by distinct pathways. Through interference with p38MAPK activity, we show that radiation-induced stress phenotypes promote genomic instability. In contrast, exposure to physiologically relevant doses of hydrogen peroxide or increasing endogenous ROS levels with a catalase inhibitor reduced the level of genomic instability. Our results implicate persistently elevated ROS following exposure to radiation as a factor contributing to genome stabilization. 相似文献
109.
The annealing of nucleic acids to (partly) complementary RNA or DNA strands is involved in important cellular processes. A variety of proteins have been shown to accelerate RNA/RNA annealing but their mode of action is still mainly uncertain. In order to study the mechanism of protein-facilitated acceleration of annealing we selected a short peptide, HIV-1 Tat(44-61), which accelerates the reaction efficiently. The activity of the peptide is strongly regulated by mono- and divalent cations which hints at the importance of electrostatic interactions between RNA and peptide. Mutagenesis of the peptide illustrated the dominant role of positively charged amino acids in RNA annealing--both the overall charge of the molecule and a precise distribution of basic amino acids within the peptide are important. Additionally, we found that Tat(44-61) drives the RNA annealing reaction via entropic rather than enthalpic terms. One-dimensional-NMR data suggest that the peptide changes the population distribution of possible RNA structures to favor an annealing-prone RNA conformation, thereby increasing the fraction of colliding RNA molecules that successfully anneal. 相似文献
110.