A unified Erd\H{o}s-P\'{o}sa theorem for cycles in graphs labelled by multiple abelian groups

In 1965, Erd\H{o}s and P\'{o}sa proved that there is a duality between the maximum size of a packing of cycles and the minimum size of a vertex set hitting all cycles. Such a duality does not hold for odd cycles, and Dejter and Neumann-Lara asked in 1988 to find all pairs ${(\ell, z)}$ of integers where such a duality holds for the family of cycles of length $\ell$ modulo $z$. We characterise all such pairs, and we further generalise this characterisation to cycles in graphs labelled with a bounded number of abelian groups, whose values avoid a bounded number of elements of each group. This unifies almost all known types of cycles that admit such a duality, and it also provides new results. Moreover, we characterise the obstructions to such a duality in this setting, and thereby obtain an analogous characterisation for cycles in graphs embeddable on a fixed compact orientable surface.Comment: 37 pages, 2 figure

The Fanconi anemia proteins FANCD2 and FANCJ interact and regulate each other's chromatin localization.

Fanconi anemia is a genetic disease resulting in bone marrow failure, birth defects, and cancer that is thought to encompass a defect in maintenance of genomic stability. Mutations in 16 genes (FANCA, B, C, D1, D2, E, F, G, I, J, L, M, N, O, P, and Q) have been identified in patients, with the Fanconi anemia subtype J (FA-J) resulting from homozygous mutations in the FANCJ gene. Here, we describe the direct interaction of FANCD2 with FANCJ. We demonstrate the interaction of FANCD2 and FANCJ in vivo and in vitro by immunoprecipitation in crude cell lysates and from fractions after gel filtration and with baculovirally expressed proteins. Mutation of the monoubiquitination site of FANCD2 (K561R) preserves interaction with FANCJ constitutively in a manner that impedes proper chromatin localization of FANCJ. FANCJ is necessary for FANCD2 chromatin loading and focus formation in response to mitomycin C treatment. Our results suggest not only that FANCD2 regulates FANCJ chromatin localization but also that FANCJ is necessary for efficient loading of FANCD2 onto chromatin following DNA damage caused by mitomycin C treatment

Analyses of the yeast Rad51 recombinase A265V mutant reveal different in vivo roles of Swi2-like factors

The Saccharomyces cerevisiae Swi2-like factors Rad54 and Rdh54 play multifaceted roles in homologous recombination via their DNA translocase activity. Aside from promoting Rad51-mediated DNA strand invasion of a partner chromatid, Rad54 and Rdh54 can remove Rad51 from duplex DNA for intracellular recycling. Although the in vitro properties of the two proteins are similar, differences between the phenotypes of the null allele mutants suggest that they play different roles in vivo. Through the isolation of a novel RAD51 allele encoding a protein with reduced affinity for DNA, we provide evidence that Rad54 and Rdh54 have different in vivo interactions with Rad51. The mutant Rad51 forms a complex on duplex DNA that is more susceptible to dissociation by Rdh54. This Rad51 variant distinguishes the in vivo functions of Rad54 and Rdh54, leading to the conclusion that two translocases remove Rad51 from different substrates in vivo. Additionally, we show that a third Swi2-like factor, Uls1, contributes toward Rad51 clearance from chromatin in the absence of Rad54 and Rdh54, and define a hierarchy of action of the Swi2-like translocases for chromosome damage repair

The Rad51 paralogs facilitate a novel DNA strand specific damage tolerance pathway

Accurate DNA replication is essential for genomic stability and cancer prevention. Homologous recombination is important for high-fidelity DNA damage tolerance during replication. How the homologous recombination machinery is recruited to replication intermediates is unknown. Here, we provide evidence that a Rad51 paralog-containing complex, the budding yeast Shu complex, directly recognizes and enables tolerance of predominantly lagging strand abasic sites. We show that the Shu complex becomes chromatin associated when cells accumulate abasic sites during S phase. We also demonstrate that purified recombinant Shu complex recognizes an abasic analog on a double-flap substrate, which prevents AP endo-nuclease activity and endonuclease-induced double-strand break formation. Shu complex DNA binding mutants are sensitive to methyl methanesulfonate, are not chromatin enriched, and exhibit increased mutation rates. We propose a role for the Shu complex in recognizing abasic sites at replication intermediates, where it recruits the homologous recombination machinery to mediate strand specific damage tolerance

Guidelines for DNA recombination and repair studies: Mechanistic assays of DNA repair processes

Genomes are constantly in flux, undergoing changes due to recombination, repair and mutagenesis. In vivo, many of such changes are studies using reporters for specific types of changes, or through cytological studies that detect changes at the single-cell level. Single molecule assays, which are reviewed here, can detect transient intermediates and dynamics of events. Biochemical assays allow detailed investigation of the DNA and protein activities of each step in a repair, recombination or mutagenesis event. Each type of assay is a powerful tool but each comes with its particular advantages and limitations. Here the most commonly used assays are reviewed, discussed, and presented as the guidelines for future studies

The removal mechanisms of titanium nitride coated steels in scratch tests.

Most previous studies on wear of coatings have been concluded, without detailed study, that coating removal occurs by debonding failure at the coating-substrate interface. However, a few researchers have suggested that failure of the coating itself and substrate deformation may also contribute to coating removal. In the present study, the roles of debonding, coating and substrate failure in coating removal are investigated for scratch tests. Single and multi pass scratch tests were performed on a set of titanium nitride (TiN) coated steels, and the resulting damage and removal behaviors are described. In addition, some finite element analysis of stress states in coated systems during scratching contact are described, focusing on the damage-governing stresses. From the experiments, it is shown that coating removal is not controlled by debonding failure alone, but rather by a combination of debonding, cracking in the coating and substrate deformation failure. Based on the stress analysis, coating damage and removal models are described graphically. These models correspond qualitatively with the coating removal processes observed in the experiments.Ph.D.Mechanical EngineeringUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/104973/1/9624655.pdfDescription of 9624655.pdf : Restricted to UM users only

Estimating the value of financial transmission rights for transmission expansion

The current situation of insufficient investment in transmission tends to weaken the advantages of a deregulated power industry. These shortages mainly arise because of the risk of not recovering the cost of investing in new lines Location Marginal prices (LMPs) and Financial Transmission Rights (FTRs) are key elements in reducing these investment risks. Market participants are able to hedge against price fluctuations caused by transmission congestion through the purchase or sale of FTRs. The value of FTRs, which is tied to the difference in prices between locations in the network, would indicate where transmission expansion should be implemented.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Binding of zinc finger protein transcription factor IIIA to its cognate DNA sequence with single UV photoproducts at specific sites and its effect on DNA repair

The relationship between DNA repair efficiency at specific locations in the binding site of the nine-zinc finger protein transcription factor IIIA (TFIIIA) and binding of its individual zinc fingers was studied. Homogeneously damaged oligonucleotides, which contained a single cis-syn cyclobutane thymine dimer (CTD) at one of six different sites in the internal control region (ICR) of the 5 S rRNA gene to generate a series of damaged DNA substrates, were prepared by chemical synthesis. Binding of TFIIIA to the substrates was assayed by measurement of dissociation constants (Kd), dissociation rates (koff), and protein-DNA contacts. The results indicated that a single CTD in the ICR does not significantly affect the Kd of TFIIIA. In contrast, CTDs at positions +55 and +72 (from the transcription start site) in the ICR markedly enhanced koff of TFIIIA from the complex. In addition, CTDs in these two sites increased methylation of the N7 of guanines (by dimethyl sulfate) in the zinc finger contacts of the ICR-TFIIIA complex. Furthermore CTDs at +55 and +72 were more efficiently removed from the complex than CTDs at other sites in the ICR by Xenopus oocyte nuclear extracts. This suggests that repair of CTDs closely correlates with changes in the binding of individual zinc fingers of the ICR-TFIIIA complex. These results have implications for the mechanism of DNA damage recognition and repair in protein-DNA complexes

Provably Secure Three-Factor-Based Mutual Authentication Scheme with PUF for Wireless Medical Sensor Networks

Wireless medical sensor networks (WMSNs) are used in remote medical service environments to provide patients with convenient healthcare services. In a WMSN environment, patients wear a device that collects their health information and transmits the information via a gateway. Then, doctors make a diagnosis regarding the patient, utilizing the health information. However, this information can be vulnerable to various security attacks because the information is exchanged via an insecure channel. Therefore, a secure authentication scheme is necessary for WMSNs. In 2021, Masud et al. proposed a lightweight and anonymity-preserving user authentication scheme for healthcare environments. We discover that Masud et al.’s scheme is insecure against offline password guessing, user impersonation, and privileged insider attacks. Furthermore, we find that Masud et al.’s scheme cannot ensure user anonymity. To address the security vulnerabilities of Masud et al.’s scheme, we propose a three-factor-based mutual authentication scheme with a physical unclonable function (PUF). The proposed scheme is secure against various security attacks and provides anonymity, perfect forward secrecy, and mutual authentication utilizing biometrics and PUF. To prove the security features of our scheme, we analyze the scheme using informal analysis, Burrows–Abadi–Needham (BAN) logic, the Real-or-Random (RoR) model, and Automated Verification of Internet Security Protocols and Applications (AVISPA) simulation. Furthermore, we estimate our scheme’s security features, computation costs, communication costs, and energy consumption compared with the other related schemes. Consequently, we demonstrate that our scheme is suitable for WMSNs