Mph1 is a member of the conserved FANCM family of DNA motor proteins that play key roles in genome maintenance processes underlying Fanconi anemia, a cancer predisposition syndrome in humans. Here, we identify Mte1 as a novel interactor of the Mph1 helicase in Saccharomyces cerevisiae. In vitro, Mte1 (Mph1-associated telomere maintenance protein 1) binds directly to DNA with a preference for branched molecules such as D loops and fork structures. In addition, Mte1 stimulates the helicase and fork regression activities of Mph1 while inhibiting the ability of Mph1 to dissociate recombination intermediates. Deletion of MTE1 reduces crossover recombination and suppresses the sensitivity of mph1Δ mutant cells to replication stress. Mph1 and Mte1 interdependently colocalize at DNA damage-induced foci and dysfunctional telomeres, and MTE1 deletion results in elongated telomeres. Taken together, our data indicate that Mte1 plays a role in regulation of crossover recombination, response to replication stress, and telomere maintenance.
BackgroundHuman activity has a profound effect on the global environment and caused frequent occurrence of climatic fluctuations. To survive, plants need to adapt to the changing environmental conditions through altering their morphological and physiological traits. One known mechanism for phenotypic innovation to be achieved is environment-induced rapid yet inheritable epigenetic changes. Therefore, the use of molecular techniques to address the epigenetic mechanisms underpinning stress adaptation in plants is an important and challenging topic in biological research. In this study, we investigated the impact of warming, nitrogen (N) addition, and warming+nitrogen (N) addition stresses on the cytosine methylation status of Leymus chinensis Tzvel. at the population level by using the amplified fragment length polymorphism (AFLP), methylation-sensitive amplified polymorphism (MSAP) and retrotransposon based sequence-specific amplification polymorphism (SSAP) techniques.Methodology/Principal FindingsOur results showed that, although the percentages of cytosine methylation changes in SSAP are significantly higher than those in MSAP, all the treatment groups showed similar alteration patterns of hypermethylation and hypomethylation. It meant that the abiotic stresses have induced the alterations in cytosine methylation patterns, and the levels of cytosine methylation changes around the transposable element are higher than the other genomic regions. In addition, the identification and analysis of differentially methylated loci (DML) indicated that the abiotic stresses have also caused targeted methylation changes at specific loci and these DML might have contributed to the capability of plants in adaptation to the abiotic stresses.Conclusions/SignificanceOur results demonstrated that abiotic stresses related to global warming and nitrogen deposition readily evoke alterations of cytosine methylation, and which may provide a molecular basis for rapid adaptation by the affected plant populations to the changed environments.
Abstract. The insulin-like growth factor binding protein-3 (IGFBP-3) gene is a structural gene responsible for the multiple effects of insulin-like growth factors (IGFs) playing a key role in mammalian growth, development and reproduction (BALE et al., 1992; HASTIE et al., 2004). Single nucleotide polymorphisms (SNPs) have been described in the bovine IGFBP3 gene which was associated with production traits, as well as in the buffalo (MACIULLA et al., 1997; PADMA et al., 2004). No polymorphism was detected in the sheep IGFBP3 gene (KUMAR et al., 2006). In present experiment most of the coding region and part of introns of IGFBP3 were scanned for SNPs in predominant goat breeds of China. Associations of SNPs of IGFBP3 with litter size and weight traits were analyzed.
Single-nucleotide polymorphisms (SNPs), microsatellites and copy number variation (CNV) were studied on the Y chromosome to understand the paternal origin and phylogenetic relationships for resource protection, rational development and utilization of the domestic Bactrian camel in China. Our sample set consisted of 94 Chinese domestic Bactrian camels from four regions (Inner Mongolia, Gansu, Qinghai and Xinjiang), we screened 29 Y-chromosome-specific loci for SNPs, analysed 40 bovine-derived microsatellite loci and measured CNVs of HSFY and SRY through Sanger sequencing, automated fluorescence-based microsatellite analysis and quantitative real-time PCR, respectively. A multicopy gene, SRY, was first found, and sequence variation was only detected in SRY in a screen of 29 loci in 13 DNA pools of individual camels. In addition, a TG repeat in the USP9Y gene was identified as the first polymorphic microsatellite in the camel Y chromosome, whereas microsatellite based on bovine sequences were not detected. The frequency of each allele varied among different populations. For the Nanjiang, Hexi and Alashan populations, a 243-bp allele was found. For the Sunite population, 241-bp, 243-bp and 247-bp alleles were detected, and the frequencies of these alleles were 22.2%, 44.5% and 33.3%, respectively; 241-bp and 243-bp alleles were found in other populations. Finally, CNVs in two Y-chromosomal genes were detected; CNV for HSFY and SRY ranged from 1 to 3 and from 1 to 9, respectively.
BackgroundEtoposide (epipodophyllotoxin) is a chemical commonly used as an anti-cancer drug which inhibits DNA synthesis by blocking topoisomerase II activity. Previous studies in animal cells have demonstrated that etoposide constitutes a genotoxic stress which may induce genomic instability including mobilization of normally quiescent transposable elements (TEs). However, it remained unknown whether similar genetically mutagenic effects could be imposed by etoposide in plant cells. Also, no information is available with regard to whether the drug may cause a perturbation of epigenetic stability in any organism.ResultsTo investigate whether etoposide could generate genetic and/or epigenetic instability in plant cells, we applied etoposide to germinating seeds of six cultivated rice (Oryza sativa L.) genotypes including both subspecies, japonica and indica. Based on the methylation-sensitive gel-blotting results, epigenetic changes in DNA methylation of three TEs (Tos17, Osr23 and Osr36) and two protein-encoding genes (Homeobox and CDPK-related genes) were detected in the etoposide-treated plants (S0 generation) in four of the six studied japonica cultivars, Nipponbare, RZ1, RZ2, and RZ35, but not in the rest japonica cultivar (Matsumae) and the indica cultivar (93-11). DNA methylation changes in the etoposide-treated S0 rice plants were validated by bisulfite sequencing at both of two analyzed loci (Tos17 and Osr36). Transpositional activity was tested for eight TEs endogenous to the rice genome in both the S0 plants and their selfed progenies (S1 and S2) of one of the cultivars, RZ1, which manifested heritable phenotypic variations. Results indicated that no transposition occurred in the etoposide-treated S0 plants for any of the TEs. Nonetheless, a MITE transposon, mPing, showed rampant mobilization in the S1 and S2 progenies descended from the drug-treated S0 plants.ConclusionsOur results demonstrate that etoposide imposes a similar genotoxic stress on plant cells as it does on animal and human cells, which may induce transgenerational genomic instability by instigating transpositional activation of otherwise dormant TEs. In addition, we show for the first time that etoposide may induce epigenetic instability in the form of altered DNA methylation patterns in eukaryotes. However, penetrance of the genotoxic effects of etoposide on plant cells, as being reflected as genetic and epigenetic instability, appears to be in a strictly genotype- and/or generation-dependent manner.
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