The Influence of Flower Color on the Foraging Selection of the Julia Butterfly, Dyras Uilia, in a Captive Habitat at the Minnesota Zoo

https://openriver.winona.edu/urc2018/1006/thumbnail.jp

Poly(adp-ribose) Polymerase: Aspects Of Its Interaction With Dna

Poly(ADP-ribose) polymerase from calf thymus was purified to near homogeneity. The use of red-agarose resulted in a rapid purification with a high yield. Purified poly(ADP-ribose) polymerase was inhibited by 1,10-phenanthroline, a metal chelating agent, at pH \u3c 8. This inhibition and the inhibition by other chelating agents suggested that this enzyme was a metalloprotein. Control experiments eliminated the possibility that the inhibition was due to the DNA-degrading properties of 1,10-phenanthroline. Atomic absorption spectroscopy showed the presence of one atom of zinc per protein molecule. Dialysis of the enzyme against buffers containing 1,10-phenanthroline resulted in the loss of activity and the coincidental removal of zinc from the enzyme. Initial rate kinetics showed that 1,10-phenanthroline was non-competitive with NAD(\u27+) and competitive with DNA. The binding of DNA to the enzyme was unaffected by the inhibitor. These results suggest a metal-containing site is involved in the interaction of DNA and poly(ADP-ribose) polymerase.;Previous reports have indicated that poly(ADP-ribose) polymerase, besides modifying various chromatin proteins, also modifies itself. The studies reported here indicate that this auto-modification inhibited the enzyme. By observing the binding of poly(ADP-ribose) polymerase to the DNA it was shown that the affinity of modified poly(ADP-ribose) polymerase for DNA was decreased. Mg(\u272+) and histone H1 appear to activate the polymerase by increasing the affinity of the auto-modified polymerase for DNA, probably by neutralizing the negative charges on poly(ADP-ribose). The coupling of poly(ADP-ribose) glycohydrolase with the polymerase reactivated the polymerase by degrading the poly(ADP-ribose) and restoring the polymerase-DNA complex. These results provided the basis for a shuttle mechanism by which proteins could be moved on and off DNA by the actions of poly(ADP-ribose) polymerase and glycohydrolase

Report on the Status of Payday Lending in California

Provides an overview of storefront and Internet payday lending in California, its effects, state and federal laws and regulations, and reform efforts. Includes recommendations for state and local policy, banking access, and consumer education

Evoking Regional Vestige - A Unique Legacy

This thesis discusses the concepts used in a series of paintings and drawings evoking an authentic view of regional environment and humanity. Included is a discussion of procedure and methodology

Preciznost sklapanja genoma bakterije Escherichia coli nakon γ-zračenja

γ-Radiation, a powerful DNA-damaging agent, can often lead to the formation of genome rearrangements. In this study, we have assessed the capacity of Escherichia coli to accurately reassemble its genome after multiple double-strand DNA breaks caused by γ-radiation. It has recently been shown that very high doses of γ-radiation or RecA protein deficiency cause erroneous chromosomal assemblies in Deinococcus radiodurans, a highly radiation-resistant bacterium. Accordingly, we have examined the accuracy of genome reassembly in both wild-type and recA strains of E. coli after exposure to the doses of γ-radiation which reduce the survival by 10^6 - to 10^7 -fold. Thirty-eight percent of wild-type survivors showed gross genome changes, most of which were found to be the consequence of the excision of e14, a 15-kb defective prophage. Only one additional type of gross genome rearrangement was detected, presumably representing the duplication of a DNA fragment. These results demonstrate an unexpectedly accurate genome reassembly in wild-type E. coli. We have detected no genome rearrangements in recA recBCD and recA recBCD sbcB mutants, suggesting that RecA-independent DNA repair in E. coli may also be accurate.Gama-zračenje je moćan agens koji oštećuje molekulu DNA i uzrokuje preraspodjelu genoma. U ovom smo radu ispitali sposobnost bakterije Escherichia coli da precizno sklopi svoj genom nakon višestrukih dvolančanih lomova DNA izazvanih γ-zračenjem. Nedavno smo dokazali da izuzetno velike doze γ-zračenja ili nedostatak proteina RecA uzrokuju pogrešno sklapanje genoma u bakteriji Deinococcus radiodurans, otpornoj na zračenje. Stoga smo istražili preciznost sklapanja genoma u divljem tipu i mutantu recA bakterije E. coli nakon izlaganja dozama γ-zračenja što smanjuju mogućnost preživljavanja stanica 10^6 do 10^7 puta. Kod 38 % stanica divljega tipa došlo je do velikih promjena u genomu, uglavnom kao posljedica izrezivanja profaga e14. Uz to, pronašli smo još samo jedan tip veće promjene u preraspodjeli genoma koji je vjerojatno posljedica udvostručenja fragmenta DNA. Rezultati pokazuju da divlji tip bakterije E. coli ima neočekivano veliku preciznost obnove genoma. U mutantima recA recBCD i recA recBCD sbcB nismo detektirali preraspodjelu genoma, što pokazuje da bi i RecA-neovisni popravak DNA u bakteriji E. coli također mogao biti vrlo precizan

Genetic analysis of transductional recombination in Escherichia coli reveals differences in the postsynaptic stages of RecBCD and RecFOR pathways

Background and purpose: Homologous recombination in Escherichia coli proceeds via two pathways, RecBCD and RecFOR, which use different enzymes for DNA end resection and loading of RecA recombinase. The postsynaptic reactions following RecA-mediated homologous pairing have mostly been studied within the RecBCD pathway. They involve RuvABC helicase/resolvase complex, RecG and RadA helicases that process recombination intermediates to produce recombinant DNA molecules. Also, RecG functionally interacts with the PriA protein in initiation of recombination-dependent replication. Here, we studied the individual and combined effects of ruvABC, recG and radA null mutations on transductional recombination in both pathways. The effect of the priA300 mutation, which acts as a suppressor of the recG mutation, was also tested. The goal was to characterize the postsynaptic stage of transductional recombination in more details, especially in the RecFOR pathway, which is less well-studied. Materials and methods: Phage P1vir-mediated transduction was used to measure recombination efficiency in a series of recombination mutants. The proA+ marker was used for selection in transductional crosses with various ΔproA recipients. Results: The ruvABC mutation moderately decreased recombination in both recombination pathways, while radA had no effect. The recG mutation reduced recombination in the RecBCD pathway but not in the RecFOR pathway. The strong recombination defect of recG radA double mutants in both pathways was completely suppressed by the priA300 mutation, and this suppression depended on the functional RuvABC complex. Conclusions: RecG and RadA proteins have a redundant role in transductional recombination via RecFOR pathway. In both recombination pathways, RecG and RadA functionally interact with PriA, probably during initiation of recombination- dependent replication

Chromosome Segregation and Cell Division Defects in Escherichia coli Recombination Mutants Exposed to Different DNA-Damaging Treatments

Homologous recombination repairs potentially lethal DNA lesions such as double-strand DNA breaks (DSBs) and single-strand DNA gaps (SSGs). In Escherichia coli, DSB repair is initiated by the RecBCD enzyme that resects double-strand DNA ends and loads RecA recombinase to the emerging single-strand (ss) DNA tails. SSG repair is mediated by the RecFOR protein complex that loads RecA onto the ssDNA segment of gaped duplex. In both repair pathways, RecA catalyses reactions of homologous DNA pairing and strand exchange, while RuvABC complex and RecG helicase process recombination intermediates. In this work, we have characterised cytological changes in various recombination mutants of E. coli after three different DNA-damaging treatments: (i) expression of I-SceI endonuclease, (ii) gamma-irradiation, and (iii) UV-irradiation. All three treatments caused severe chromosome segregation defects and DNA-less cell formation in the ruvABC, recG, and ruvABC recG mutants. After I-SceI expression and gamma-irradiation, this phenotype was efficiently suppressed by the recB mutation, indicating that cytological defects result mostly from incomplete DSB repair. In UV-irradiated cells, the recB mutation abolished cytological defects of recG mutants and also partially suppressed the cytological defects of ruvABC recG mutants. However, neither recB nor recO mutation alone could suppress the cytological defects of UV- irradiated ruvABC mutants. The suppression was achieved only by simultaneous inactivation of the recB and recO genes. Cell survival and microscopic analysis suggest that chromosome segregation defects in UV-irradiated ruvABC mutants largely result from defective processing of stalled replication forks. The results of this study show that chromosome morphology is a valuable marker in genetic analyses of recombinational repair in E. coli

Variations in Adipokine Genes AdipoQ, Lep, and LepR are Associated with Risk for Obesity-Related Metabolic Disease: The Modulatory Role of Gene-Nutrient Interactions

Obesity rates are rapidly increasing worldwide and facilitate the development of many related disease states, such as cardiovascular disease, the metabolic syndrome, type 2 diabetes mellitus, and various types of cancer. Variation in metabolically important genes can have a great impact on a population's susceptibility to becoming obese and/or developing related complications. The adipokines adiponectin and leptin, as well as the leptin receptor, are major players in the regulation of body energy homeostasis and fat storage. This paper summarizes the findings of single nucleotide polymorphisms in these three genes and their effect on obesity and metabolic disease risk. Additionally, studies of gene-nutrient interactions involving adiponectin, leptin, and the leptin receptor are highlighted to emphasize the critical role of diet in susceptible populations