Showing papers on "Nuclear DNA published in 2003"
TL;DR: The mitochondrial respiratory chain has the crucial function of supplying the cell with energy in the form of ATP, and mutations affecting this chain can arise in mitochondrial or nuclear DNA and cause diseases known as mitochondrial encephalomyopathies.
Abstract: The mitochondrial respiratory chain has the crucial function of supplying the cell with energy in the form of ATP. Mutations affecting this chain can arise in mitochondrial or nuclear DNA and cause diseases known as mitochondrial encephalomyopathies. Because the rules of inheritance of mitochondrial and nuclear DNA differ considerably, these brain–muscle syndromes often have unpredictable clinical and genetic features.
1,489 citations
TL;DR: Because trout and human nuclei are often used as internal reference standards to determine genome size in animals and plants, the results published by Thomas et al. (1) need correction to avoid serious mistakes.
Abstract: NUCLEAR DNA CONTENT AND GENOME SIZE OF TROUT AND HUMAN In their recent paper, Thomas et al. (1) discussed design, resolution, sensitivity, and reproducibility of the National Aeronautics and Space Administration/American Cancer Society flow cytometer. The results of their study demonstrated high stability and sensitivity of the instrument, which is suitable for detection of near-diploid tumor cells. Although the performance of the instrument is impressive, we believe that Thomas et al. made serious errors in calculating the DNA contents of trout and human. To estimate the DNA content of human cells in picograms of DNA, the authors used trout red blood cell nuclei as the internal reference standard and assumed 2.37 pg of DNA for a trout nucleus. With this value, the DNA contents of human female and male nuclei were estimated to be equal to 3.77 and 3.70 pg of DNA, respectively. The new estimates for trout and human differ drastically from previous ones, which range from 4.9 to 6.3 pg for various species of trout (2–5) and from 6.0 to 7.0 pg for human (5–9). Because trout and human nuclei are often used as internal reference standards to determine genome size in animals and plants (5,10,11), the results published by Thomas et al. (1) need correction to avoid serious mistakes. Careful reading of the paper showed that the DNA content of trout (the authors did not specify the species) was derived after determining the ratio of mean DNA content of human male to trout to be 1.565. The DNA amount of the human nucleus, 3.70 pg, was calculated with the assumption that there are 6.162 10 nucleotides for the human male nucleus and that a mean nucleotide molecular weight of 360 g/mol. We believe these data are not correct.
1,014 citations
TL;DR: This PCR-based assay not only enables accurate determination of mtDNA relative to nuclear DNA but also has the potential to quantify accurately any DNA sequence in relation to any other.
Abstract: Deletions in mitochondrial DNA (mtDNA) accumulate with age in humans without overt mitochondriopathies, but relatively limited attention has been devoted to the measurement of the total number of mtDNA molecules per cell during ageing. We have developed a precise assay that determines mtDNA levels relative to nuclear DNA using a PCR-based procedure. Quantification was performed by reference to a single recombinant plasmid standard containing a copy of each target DNA sequence (mitochondrial and nuclear). Copy number of mtDNA was determined by amplifying a short region of the cytochrome b gene (although other regions of mtDNA were demonstrably useful). Nuclear DNA content was determined by amplification of a segment of the single copy β-globin gene. The copy number of mtDNA per diploid nuclear genome in myocardium was 6970 ± 920, significantly higher than that in skeletal muscle, 3650 ± 620 (P = 0.006). In both human skeletal muscle and myocardium, there was no significant change in mtDNA copy number with age (from neonates to subjects older than 80 years). This PCR-based assay not only enables accurate determination of mtDNA relative to nuclear DNA but also has the potential to quantify accurately any DNA sequence in relation to any other.
330 citations
TL;DR: Findings show that mitochondrial polymorphisms are not as neutral as was previously believed and exchanges of mtDNA may produce phenotypes outside the range of scores observed in the original mitochondrial and nuclear combinations.
Abstract: Several lines of evidence indicate an association between mitochondrial DNA (mtDNA) and the functioning of the nervous system. As neuronal development1,2 and structure3,4,5 as well as axonal and synaptic activity6,7 involve mitochondrial genes, it is not surprising that most mtDNA diseases are associated with brain disorders8,9. Only one study has suggested an association between mtDNA and cognition10, however. Here we provide direct evidence of mtDNA involvement in cognitive functioning. Total substitution of mtDNA was achieved by 20 repeated backcrosses in NZB/BlNJ (N) and CBA/H (H) mice with different mtDNA origins. All 13 mitochondrial genes were expressed in the brains of the congenic quartet. In interaction with nuclear DNA (nDNA), mtDNA modified learning, exploration, sensory development and the anatomy of the brain. The effects of mtDNA substitution persisted with age, increasing in magnitude as the mice got older. We observed different effects with input of mtDNA from N versus H mice, varying according to the phenotypes. Exchanges of mtDNA may produce phenotypes outside the range of scores observed in the original mitochondrial and nuclear combinations. These findings show that mitochondrial polymorphisms are not as neutral as was previously believed.
192 citations
TL;DR: A role for nuclear DNA encoded mitochondrial proteins in carcinogenesis is pointed to, underscoring their potential as targets for therapy while highlighting the need for full characterization of the mitochondrial proteome.
Abstract: Laser capture microdissection was combined with reverse phase protein lysate arrays to quantitatively analyze the ratios of mitochondrial encoded cytochrome c oxidase subunits to nuclear encoded cytochrome c oxidase subunits, and to correlate the ratios with malignant progression in human prostate tissue specimens. Cytochrome c oxidase subunits I-III comprise the catalytic core of the enzyme and are all synthesized from mitochondrial DNA. The remaining subunits (IV-VIII) are synthesized from cellular nuclear DNA. A significant (P < 0.001, 30/30 prostate cases) shift in the relative concentrations of nuclear encoded cytochrome c oxidase subunits IV, Vb, and VIc compared to mitochondrial encoded cytochrome c oxidase subunits I and II was noted during the progression of prostate cancer from normal epithelium through premalignant lesions to invasive carcinoma. Significantly, this shift was discovered to begin even in the premalignant stage. Reverse phase protein lysate array-based observations were corroborated with immunohistochemistry, and extended to a few human carcinomas in addition to prostate. This analysis points to a role for nuclear DNA encoded mitochondrial proteins in carcinogenesis; underscoring their potential as targets for therapy while highlighting the need for full characterization of the mitochondrial proteome.
171 citations
TL;DR: Production of ROS is markedly enhanced in many pathological conditions in which the respiratory chain is impaired, and mitochondrial DNA, which is essential for execution of normal oxidative phosphorylation, is more oxidatively damaged than is nuclear DNA.
Abstract: Mitochondria produce reactive oxygen species (ROS) under physiological conditions in association with activity of the respiratory chain in aerobic ATP production. The production of ROS is essentially a function of O2 consumption. Hence, increased mitochondrial activity per se can be an oxidative stress to cells. Furthermore, production of ROS is markedly enhanced in many pathological conditions in which the respiratory chain is impaired. Because mitochondrial DNA, which is essential for execution of normal oxidative phosphorylation, is located in proximity to the ROS-generating respiratory chain, it is more oxidatively damaged than is nuclear DNA. Cumulative damage of mitochondrial DNA is implicated in the aging process and in the progression of such common diseases as diabetes, cancer, and heart failure.
167 citations
TL;DR: This study sequenced 50 noncoding, nonrepetitive DNA segments randomly chosen from the nuclear genome in 9 bonobos and 17 chimpanzees and found that the pi value for bonobos is only 0.078%, even somewhat lower than that for humans for the same 50 segments, which is puzzling.
Abstract: Comparison of the levels of nucleotide diversity in humans and apes may provide much insight into the mechanisms of maintenance of DNA polymorphism and the demographic history of these organisms. In the past, abundant mitochondrial DNA (mtDNA) polymorphism data indicated that nucleotide diversity (pi) is more than threefold higher in chimpanzees than in humans. Furthermore, it has recently been claimed, on the basis of limited data, that this is also true for nuclear DNA. In this study we sequenced 50 noncoding, nonrepetitive DNA segments randomly chosen from the nuclear genome in 9 bonobos and 17 chimpanzees. Surprisingly, the pi value for bonobos is only 0.078%, even somewhat lower than that (0.088%) for humans for the same 50 segments. The pi values are 0.092, 0.130, and 0.082% for East, Central, and West African chimpanzees, respectively, and 0.132% for all chimpanzees. These values are similar to or at most only 1.5 times higher than that for humans. The much larger difference in mtDNA diversity than in nuclear DNA diversity between humans and chimpanzees is puzzling. We speculate that it is due mainly to a reduction in effective population size (N(e)) in the human lineage after the human-chimpanzee divergence, because a reduction in N(e) has a stronger effect on mtDNA diversity than on nuclear DNA diversity. Sequence data from this article have been deposited with the GenBank Data libraries under accession nos. AY 275957-AY 277244.
158 citations
TL;DR: It is demonstrated that in rho(0) cells the REV1, REV3 and REV7 gene products, all implicated in error-prone translesion DNA synthesis (TLS), mediate mutagenesis in the nuclear genome.
Abstract: Using Saccharomyces cerevisiae as a model organism, we analyzed the consequences of disrupting mitochondrial function on mutagenesis of the nuclear genome. We measured the frequency of canavanine-resistant colonies as a measure of nuclear mutator phenotype. Our data suggest that mitochondrial dysfunction leads to a nuclear mutator phenotype (i) when oxidative phosphorylation is blocked in wild-type yeast at mitochondrial complex III by antimycin A and (ii) in mutant strains lacking the entire mitochondrial genome (rho(0)) or those with deleted mitochondrial DNA (rho(-)). The nuclear mutation frequencies obtained for antimycin A-treated cells as well as for rho(-) and rho(0) cells were approximately 2- to 3-fold higher compared to untreated control and wild-type cells, respectively. Blockage of oxidative phosphorylation by antimycin A treatment led to increased intracellular levels of reactive oxygen species (ROS). In contrast, inactivation of mitochondrial activity (rho(-) and rho(0)) led to decreased intracellular levels of ROS. We also demonstrate that in rho(0) cells the REV1, REV3 and REV7 gene products, all implicated in error-prone translesion DNA synthesis (TLS), mediate mutagenesis in the nuclear genome. However, TLS was not involved in nuclear DNA mutagenesis caused by inhibition of mitochondrial function by antimycin A. Together, our data suggest that mitochondrial dysfunction is mutagenic and multiple pathways are involved in this nuclear mutator phenotype.
144 citations
TL;DR: The authors' data support the hypothesis that the insular selection pressures in Macaronesia favour small C-values and genome sizes and both positive and negative correlations between infrageneric nuclear DNA amount variation and environmental conditions on Tenerife were also found in several genera.
137 citations
TL;DR: Results show that ancient single-copy nuclear DNA can be recovered from warm, arid climates, showing that nuclear DNA preservation is not restricted to cold climates.
130 citations
TL;DR: The results show that moa were characterized by extreme reverse sexual dimorphism and as a result they have been able to clarify the number of moa species and illustrates that single-locus nuclear DNA sequences can be consistently recovered from ancient material.
Abstract: Ancient DNA studies have typically used multi-copy mitochondrial DNA sequences1,2. This is largely because single-locus nuclear genes have been difficult to recover from sub-fossil material3, restricting the scope of ancient DNA research. Here, we have isolated single-locus nuclear DNA markers to assign the sex of 115 extinct moa and, in combination with a mitochondrial DNA phylogeny, tested competing hypotheses about the specific status of moa taxa. Moa were large ratite birds that showed extreme size variation both within and among species4. For some taxa, this large variation was hypothesized to represent sexual dimorphism, while for others it was argued to reflect the existence of different species5. Our results show that moa were characterized by extreme reverse sexual dimorphism and as a result we have been able to clarify the number of moa species. For example, we show that the three recognized ‘species’ of Dinornis comprised only two monophyletic groups and that two of these ‘species’ comprised individuals of one sex only. This study also illustrates that single-locus nuclear DNA sequences can be consistently recovered from ancient material.
TL;DR: A reliable DNA extraction method for extra virgin olive oil has been defined, as far as both quantity and quality are concerned, and the possibility of using this DNA for fingerprinting the original cultivar has been demonstrated.
TL;DR: A patient is characterized with a de novo nucleic acid transfer from the mitochondrial to the nuclear genome, a transfer that is responsible for a sporadic case of Pallister-Hall syndrome, a condition usually inherited in an autosomal dominant fashion, to demonstrate that de noovo mitochondrial-nuclear transfer of nucleic Acid is a novel mechanism of human inherited disease.
Abstract: Transfer of nucleic acid from cytoplasmic organelles to the nuclear genome is a well-established mechanism of evolutionary change in eukaryotes. Such transfers have occurred throughout evolution, but so far, none has been shown unequivocally to occur de novo to cause a heritable human disease. We have characterized a patient with a de novo nucleic acid transfer from the mitochondrial to the nuclear genome, a transfer that is responsible for a sporadic case of Pallister-Hall syndrome, a condition usually inherited in an autosomal dominant fashion. This mutation, a 72-bp insertion into exon 14 of the GLI3 gene, creates a premature stop codon and predicts a truncated protein product. Both the mechanism and the cause of the mitochondrial-nuclear transfer are unknown. Although the conception of this patient was temporally and geographically associated with high-level radioactive contamination following the Chernobyl accident, this case cannot, on its own, be used to establish a causal relationship between radiation exposure and this rare type of mutation. Thus, for the time being, it must be considered as an intriguing coincidence. Nevertheless, these data serve to demonstrate that de novo mitochondrial-nuclear transfer of nucleic acid is a novel mechanism of human inherited disease.
TL;DR: An Arabidopsis cell-free system is developed that can be used to monitor biochemical and morphological changes in isolated nuclei that are associated with PCD and suggests the presence of an Mg2+-dependent nuclease activity in the intermembrane space is responsible for the former in vitro activity.
Abstract: The key role for mitochondria in mammalian apoptosis, a form of programmed cell death (PCD), is well established, but a similar role for plant mitochondria is just emerging. In order to unravel the molecular mechanisms linking plant mitochondria to the downstream events of PCD, we have developed an Arabidopsis cell-free system that can be used to monitor biochemical and morphological changes in isolated nuclei that are associated with PCD. Using this system, two activities that resulted in nuclear DNA degradation could be distinguished, both of which were facilitated by the addition of mitochondria. One activity mediated the generation of 30 kb DNA fragments within 3 h and chromatin condensation within 6 h, when nuclei were incubated with mitochondria alone. The second activity required cytosolic extract in addition to mitochondria and resulted in oligonucleosome-sized DNA cleavage after >12 h. Submitochondrial fractionation and pharmacological studies suggested the presence of an Mg2+-dependent nuclease activity in the intermembrane space, which is responsible for the former in vitro activity. The evolutionary conservation of the role of mitochondria in PCD in animals and plants is discussed.
TL;DR: The amount of nuclear DNA extracted from teeth of 279 individual red fox Vulpes vulpes collected over a period spanning the last three decades was determined by quantitative polymerase chain reaction (PCR); the success of PCR amplification across four examined canine microsatellites over time was dependent on fragment size.
Abstract: The amount of nuclear DNA extracted from teeth of 279 individual red fox Vulpes vulpes collected over a period spanning the last three decades was determined by quantitative polymerase chain reaction (PCR). Although teeth were autoclaved during initial collection, 73.8% of extracts contained sufficient DNA concentration (> 5 pg/ micro L) suitable for reliable microsatellite genotyping but the quantity of nuclear DNA decayed significantly over time in a nonlinear pattern. The success of PCR amplification across four examined canine microsatellites over time was dependent on fragment size. By including data from two different tests for human contamination and from frequencies of allelic dropout and false alleles, the methodological constraints of population genetic studies using microsatellite loci amplified from historic DNA are discussed.
TL;DR: Findings indicate that EndoG is essential during early embryogenesis and plays a critical role in normal apoptosis and nuclear DNA fragmentation.
Abstract: Endonuclease G (EndoG) is a nuclear-encoded mitochondrial protein reported to be important for both nuclear DNA fragmentation during apoptosis and mitochondrial DNA replication. To evaluate the in vivo function of EndoG, we have investigated the effects of EndoG deficiency in cells and mice. We found that EndoG homozygous mutant embryos die between embryonic days 2.5 and 3.5. Mitochondrial DNA copy numbers in ovulated oocytes from EndoG heterozygous mutant and wild-type mice are similar, suggesting that EndoG is involved in a cellular function unrelated to mitochondrial DNA replication. Interestingly, we found that cells from EndoG heterozygous mutant mice exhibit increased resistance to both tumor necrosis factor α- and staurosporine-induced cell death. Moreover, spontaneous cell death of spermatogonia in EndoG heterozygous mutant mice is significantly reduced compared with wild-type mice. DNA fragmentation is also reduced in EndoG+/- thymocytes and splenocytes compared with wild-type cells, as well as in EndoG+/- thymus in vivo compared with that of the wild-type mice, on activation of apoptosis. These findings indicate that EndoG is essential during early embryogenesis and plays a critical role in normal apoptosis and nuclear DNA fragmentation.
TL;DR: A comparison of allozyme and mitochondrial DNA (mtDNA) polymorphism was performed on sympatric and allopatric populations of these two tilapia species, Oreochromis niloticus and O. aureus, pointing out the risk of misinterpretation of mtDNA or nuclear DNA data when only one single class of marker is used.
Abstract: Introgressive hybridization has an important evolutionary significance in terms of gene diversity and speciation. Among the major groups of vertebrates, fish show a strong propensity to hybridize. In order to highlight the possible occurrence of gene flow between two tilapia species, Oreochromis niloticus and O. aureus, a comparison of allozyme and mitochondrial DNA (mtDNA) polymorphism was performed on sympatric and allopatric populations of these two species. Nuclear data were congruent with the morphological identification of O. niloticus and O. aureus populations. In opposition, the mtDNA analysis resulted in two strictly differentiated groups which did not follow the morphological and nuclear DNA classification. The first group consisted of East African O. niloticus populations and the second included all the O. aureus populations and the West African O. niloticus populations. Moreover, in some cases, the same sequences were detected in both species. These data strongly support a differential introgression of mtDNA from O. aureus to O. niloticus involving all the West African area. This work points out the risk of misinterpretation of mtDNA or nuclear DNA data when only one single class of marker is used.
TL;DR: The accumulation of 8-oxo-dG in the mitochondrial DNA rather than in nuclear DNA is likely to be involved in the pathogenic responses such as necrosis of renal tubular cells during I/R injury of the kidney, together with an altered level of OGG1 expression.
TL;DR: It is proposed that differences between sexes are initially determined by differential methylation in nuclear DNA between females and males, driving Muller's ratchet.
Abstract: Why are there two sexes in certain species, instead of one hermaphroditic sex? Why are Y chromosomes shorter than X chromosomes, but only in certain lineages? I propose that differences between sexes are initially determined by differential methylation in nuclear DNA between females and males, driving Muller's ratchet. Methylation of promoters suppresses transcription, including loci coding for gamete production, thereby converting hermaphroditic individuals into females or males. Differential methylation of sex chromosomes suppresses recombination and increases mutation rate, thereby geometrically increasing the speed of Muller's ratchet. Higher mutability of methylated nucleotides plus loss of sex-determining function of previously methylated nucleotides provides selective pressure to excise these loci, resulting in shorter Y or W chromosomes. Derived lineages usually have more methylation than do ancestral ones, and hence have relatively shorter sex chromosomes. Methylation canalizes dioecy and degeneration of sex chromosomes. Latter stages of sex chromosome evolution may have occurred via other mechanisms, for example sexually antagonistic genes or chromosomal rearrangements. A few aberrant derived lineages lost most methylation, and their sex determination and sex chromosomes may have evolved via other means. Differential methylation provides a mechanism for early evolution of dioecy in anisogamous sexual diploid eukaryotes and of sex chromosomes in metazoans. © 2003 The Linnean Society of London, Biological Journal of the Linnean Society, 2003, 80, 353–368.
TL;DR: P phylogenetic analyses show that C. antiquitatis is most closely related to one of the three extant Asian rhinoceros species, Dicerorhinus sumatrensis, and establishes that the degraded nature of ancient DNA does not completely protect ancient DNA studies based on mitochondrial data from the problems associated with nuclear inserts.
TL;DR: Oxidative phosphorylation, i.e., ATP synthesis by the oxygen-consuming respiratory chain (RC), supplies most organs and tissues with a readily usable energy source, being functional before birth.
Abstract: Oxidative phosphorylation, i.e., ATP synthesis by the oxygen-consuming respiratory chain (RC), supplies most organs and tissues with a readily usable energy source, being functional before birth. Consequently, RC deficiencies can theoretically give rise to any symptom, in any organ or tissue, at any age and with any mode of inheritance, because of the twofold genetic origin of RC components (nuclear DNA and mitochondrial DNA). It was long wrongly considered that RC disorders originate from mutations of mitochondrial DNA, because for a long time only mutations or deletions of mitochondrial DNA were identified. However, the number of known disease-causing mutations in nuclear genes is steadily growing. These genes encode the various subunits of each complex, ancillary proteins functioning at different stages of holoenzyme biogenesis, including transcription, translation, chaperoning, addition of prosthetic groups, and protein assembly, and various enzymes involved in mitochondrial DNA metabolism.
TL;DR: The effect of exercise on DNA damage appears to be related to the intensity of the exercise, and dietary restriction extends lifespan and is associated with reduced levels of damage to mitochondrial and nuclear DNA.
Abstract: Oxidative damage to DNA increases with age in several tissues and animal models, and mitochondrial DNA has a higher level of oxidative damage than nuclear DNA. Dietary restriction extends lifespan and is associated with reduced levels of damage to mitochondrial and nuclear DNA. The effect of exercise on DNA damage appears to be related to the intensity of the exercise.
Journal Article•
TL;DR: It is believed that the increase in sensitivity to DNA damage by overexpression of nuclear MPG is because of an imbalance in the BER pathway, and an even greater increase in cell sensitivity is observed when mitochondrial DNA is targeted.
Abstract: The DNA base excision repair (BER) pathway is responsible for the repair of alkylation and oxidative DNA damage. The short-patch BER pathway, beginning with the simple glycosylase N-methylpurine DNA glycosylase (MPG), is responsible for the removal of damaged bases such as 3-methyladenine and 1,N(6)-ethenoadenine from the DNA after alkylation or oxidative DNA damage. The resulting apurinic site is further processed by the other members in the pathway, resulting in the insertion of the correct nucleotide. If apurinic sites accumulate, they are mutagenic and cytotoxic to the cell. To evaluate its efficacy in sensitizing breast cancer cells to chemotherapy, MPG has been overexpressed in the breast cancer cell line, MDA-MB231. With MPG overexpression, an increase in DNA damage and increased cytotoxicity to methyl methanesulfonate as well as increased apoptosis levels was observed in these cells. Because mitochondrial DNA has been shown to be more sensitive to DNA damage than nuclear DNA, a construct containing mitochondrial-targeted MPG using the human manganese superoxide dismutase mitochondrial-targeting sequence was made. Overexpression of the mitochondrially targeted MPG dramatically increased the breast cancer cells' sensitivity to methyl methanesulfonate. In conclusion, we believe that the increase in sensitivity to DNA damage by overexpression of nuclear MPG is because of an imbalance in the BER pathway, and an even greater increase in cell sensitivity is observed when mitochondrial DNA is targeted.
TL;DR: Gossypium gossypioides provides a striking example of the previously unsuspected chimeric nature of some plant genomes and the resulting phylogenetic complexity produced by multiple historical reticulation events.
Abstract: The Mexican cotton Gossypium gossypioidesis a perplexing entity, with conflicting morphological, cyto- genetic, and molecular evidence of its phylogenetic affinity to other American cottons. We reevaluated the evolutionary history of this enigmatic species using 16.4 kb of DNA sequence. Phylogenetic analyses show that chloroplast DNA (7.3 kb), nuclear ribosomal internal transcribed spacers (ITS; 0.69 kb), and unique nuclear genes (8.4 kb) yield conflicting resolutions for G. gossypioides. Eight low-copy nuclear genes provide a nearly unanimous resolution of G. gossypioides as the basalmost American diploid cotton, whereas cpDNA sequences resolve G. gossypioides deeply nested within the American diploid clade sister to Peruvian G. raimondii, and ITS places G. gossypioides in an African (rather than an American) clade. These data, in conjunction with previous evidence from the repetitive fraction of the genome, implicate a complex history for G. gossypioides possibly involving temporally separated introgression events from genetically divergent cottons that are presently restricted to different hemispheres. Based on repetitive nuclear DNA, it appears that G. gossypioidesexperienced nuclear introgression from an African species shortly after divergence from the remainder of the American assemblage. More recently, hybridization with a Mexican species may have resulted in cpDNA introgression, and possibly a second round of cryptic nuclear introgression. Gossypium gossypioides provides a striking example of the previously unsuspected chimeric nature of some plant genomes and the resulting phylogenetic complexity produced by multiple historical reticulation events.
TL;DR: The results strongly suggest that inducible DNA BER constitutes an important endogenous mechanism that protects brain against ischemia-induced oxidative neuronal injury.
Abstract: To determine the role of oxidative DNA damage and repair in brain injury after focal ischemia and reperfusion, the authors investigated DNA base damage and DNA base excision repair (BER) capacity, the predominant repair mechanism for oxidative DNA lesions, in the rat model of temporary middle cerebral artery occlusion. Contents of 8-hydroxyl-2′-deoxyguanosine (8-oxodG) and apurinic/apyrimidinic abasic site (AP site), hallmarks of oxidative DNA damage, were quantitatively measured in nuclear DNA extracts from brains 0.25 to 72 hours after 1 hour of middle cerebral artery occlusion. In parallel to the detection of DNA lesions, the capacity for 8-oxodG- or AP site-dependent DNA repair synthesis was measured in nuclear protein extracts using specific in vitro DNA repair assays. After postischemic reperfusion, the levels of 8-oxodG and AP sites were markedly increased in ischemic tissues. In frontal/parietal cortex, regions that survived ischemia, 8-oxodG and AP sites were efficiently repaired during reperfusi...
TL;DR: The aim of the MitoDrome database is to annotate the Drosophila melanogaster nuclear genes coding for mitochondrial proteins in order to contribute to the functional characterization of nuclear genes coded for mitochondrion proteins and to knowledge of gene diseases related to mitochondrial dysfunctions.
Abstract: Mitochondria are organelles present in the cytoplasm of most eukaryotic cells; although they have their own DNA, the majority of the proteins necessary for a functional mitochondrion are coded by the nuclear DNA and only after transcription and translation they are imported in the mitochondrion as proteins. The primary role of the mitochondrion is electron transport and oxidative phosphorylation. Although it has been studied for a long time, the interest of researchers in mitochondria is still alive thanks to the discovery of mitochondrial role in apoptosis, aging and cancer. Aim of the MitoDrome database is to annotate the Drosophila melanogaster nuclear genes coding for mitochondrial proteins in order to contribute to the functional characterization of nuclear genes coding for mitochondrial proteins and to knowledge of gene diseases related to mitochondrial dysfunctions. Indeed D. melanogaster is one of the most studied organisms and a model for the Human genome. Data are derived from the comparison of Human mitochondrial proteins versus the Drosophila genome, ESTs and cDNA sequence data available in the FlyBase database. Links from the MitoDrome entries to the related homologous entries available in MitoNuC will be soon imple-mented. The MitoDrome database is available at http://bighost.area.ba.cnr.it/BIG/MitoDrome. Data are organised in a flat-file format and can be retrieved using the SRS system.
TL;DR: The recent report of a man with his father's mitochondria suggests a rethink of mitochondrial evolutionary dynamics in humans might be necessary.
Abstract: Mitochondrial DNA is the primary tool in the investigation of recent evolutionary history, particularly for uncovering human origins and expansion. Maternal inheritance of mitochondria enables models of population history to be much simpler that those needed for the analysis of nuclear DNA. The recent report of a man with his father's mitochondria suggests a rethink of mitochondrial evolutionary dynamics in humans might be necessary.
TL;DR: By interrogating a library of ordered YAC clones, this work provides evidence for a chromosomal copy of the rDNA on chromosome 4, and suggests that this locus may provide master copies for the stable transmission of the extrachromosomal elements.
Abstract: Ribosomal RNAs (rRNAs) are encoded by multicopy families of identical genes. In Dictyostelium and other protists, the rDNA is carried on extrachromosomal palindromic elements that comprise up to 20% of the nuclear DNA. We present the sequence of the 88 kb Dictyostelium rDNA element, noting that the rRNA genes are likely to be the only transcribed regions. By interrogating a library of ordered YAC clones, we provide evidence for a chromosomal copy of the rDNA on chromosome 4. This locus may provide master copies for the stable transmission of the extrachromosomal elements. The extrachromosomal elements were also found to form chromosome-sized clusters of DNA within nuclei of nocodazole-treated cells arrested in mitosis. These clusters resemble true chromosomes and may allow the efficient segregation of the rDNA during mitosis. These rDNA clusters may also explain the cytological observations of a seventh chromosome in this organism.
TL;DR: The yeast mitochondrial protein Abf2p was shown to be sufficient to compact linear dsDNA, without the benefit of supercoiling, using optical and atomic force microscopy single molecule techniques.
TL;DR: The results suggest that hybridization may have occurred during diversification of Fagopyrum species in the urophyllum group, and that F. rubifolium is possibly allotetraploid species.
Abstract: We performed phylogenetic analyses of Fagopyrum species in the urophyllum group based on nucleotide sequences of two nuclear genes, FLORICAULA/LEAFY (FLO/LFY) and AGAMOUS (AG), and three segments of chloroplast DNA (cpDNA), rbcL-accD, trnK intron, and trnC-rpoB spacer. The FLO/LFY and AG sequences turned out to be phylogenetically more informative at the intrageneric level than the cpDNA sequences. Congruence among these gene trees, inferred by a maximum-likelihood (ML) method, demonstrated that topologies were partially incongruent between the nuclear and chloroplast DNA phylogenies. The nuclear DNA sequence data supported a monophyletic relation of F. statice, F. gilesii, and F. jinshaense, whereas the former two species formed another monophyletic relation with the F. capillatum-F. gracilipes-F. gracilipedoides-F. rubifolium clade excluding F. jinshaense in the synthetic cpDNA phylogeny. In addition, two divergent sequences of FLO/LFY were found in F. rubifolium (tetraploid). One of these was sister to F. gracilipedoides and another was sister to F. statice, and a monophyletic relation of these two genes was rejected by a bootstrap analysis. These results suggest that hybridization may have occurred during diversification of Fagopyrum species in the urophyllum group, and that F. rubifolium is possibly allotetraploid species.