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The genetic stability of every living organism depends on accurate DNA replication and repair systems. Here, we investigated the mismatch repair (MMR) gene MshA and how it impacts virulence and the evolution of azole resistance. We examined gene variation in 62 environmental and clinical strains. We have observed 12 strains with variants (18.2%), and 8 strains among them showed missense variants. We demonstrated that null mutants are haploid and have conserved karyotypes with discrete gross chromosomal rearrangements. The Δ strains are not sensitive to several DNA-damaging agents. The lack of caused a significant reduction of virulence of in a neutropenic murine model of invasive pulmonary aspergillosis and in the invertebrate alternative model Wild-type and Δ populations did not show any significant changes in drug resistance acquisition after they were transferred 10 times in minimal medium in the absence of any stress. However, these populations rapidly acquired virulence in the Δ background and high levels of resistance to posaconazole in the presence of this drug (at least 200-fold-higher levels of resistance than those derived from the wild-type strain). Taken together, these results suggest that genetic instability caused by Δ mutations can confer an adaptive advantage, mainly increasing posaconazole resistance and virulence acquisition. Invasive aspergillosis (IA) has emerged as one of the most common life-threatening fungal diseases in immunocompromised patients, with mortality rates as high as 90%. Systemic fungal infections such as IA are usually treated with triazoles; however, epidemiological research has shown that the prevalence of azole-resistant isolates has increased significantly over the last decade. There is very little information about the importance of genomic stability for population structure, azole resistance, and virulence. Here, we decided to investigate whether the mismatch repair system could influence azole resistance and virulence, focusing on one of the components of this system, Although the mutation frequency of (the homologue) is low in environmental and clinical isolates, our results indicate that loss of function can provide increased azole resistance and virulence when selected for. These results demonstrate the importance of genetic instability in as a possible mechanism of evolving azole resistance and establishing fitness in the host.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6686229 | PMC |
http://dx.doi.org/10.1128/mSphere.00416-19 | DOI Listing |
Protein Sci
January 2025
Department of Chemistry and Biochemistry, Loyola University Chicago, Chicago, Illinois, USA.
Antimicrobial resistance is a significant cause of mortality globally due to infections, a trend that is expected to continue to rise. As existing treatments fail and new drug discovery slows, the urgency to develop novel antimicrobial therapeutics grows stronger. One promising strategy involves targeting bacterial systems exclusive to pathogens, such as the transcription regulator protein GabR.
View Article and Find Full Text PDFMol Biol Rep
December 2024
ICAR - Indian Institute of Pulses Research, Regional Station, Khordha, 752055, India.
Background: Charcoal Rot (CR) poses a significant threat to mung bean crops by reducing yield, making the development of resistant varieties crucial for stable production and food security. This study evaluated 19 newly identified mung bean landraces using biochemical traits and SSR markers, revealing genetic variability, CR disease reactions, and traits influencing yield and resistance, which provide valuable insights for breeding CR-resistant, high-yielding varieties.
Methods And Results: Mung bean landraces were evaluated for their response to CR using 4 biochemical parameters, and 10 SSR markers to assess genetic variability and disease resistance.
Oncol Rep
February 2025
Department of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
BH3 mimetics are small‑molecule inhibitors of the antiapoptotic Bcl‑2 family and have therapeutic efficacy against hematological malignancies. BH3 mimetic A‑1331852 suppresses colorectal cancer cell proliferation. Progressive resistance to the widely used anticancer agent fluorouracil (5‑FU) is a key reason for colorectal cancer recurrence; therefore, the present study tested if A‑1331852 can suppress the proliferation of 5‑FU‑resistant colorectal cancer cells.
View Article and Find Full Text PDFAntimicrob Agents Chemother
December 2024
Department of Pediatrics, Carver College of Medicine, The University of Iowa, Iowa City, Iowa, USA.
is the second most common cause of invasive candidiasis and is widely known to have reduced susceptibility to fluconazole relative to many other spp. Upc2A is a transcription factor that regulates ergosterol biosynthesis gene expression under conditions of sterol stress such as azole drug treatment or hypoxia. Through an microevolution experiment, we found that loss-of-function mutants of the ATF/CREB transcription factor suppresses the fluconazole hyper-susceptibility of the ∆ mutant.
View Article and Find Full Text PDFClinics (Sao Paulo)
December 2024
Department of Emergency, Zhejiang Jinhua Guangfu Tumor Hospital, Zhejiang, PR China.
Objective: Based on Toll Like Receptor 4 (TLR4)/Nuclear Factor-κB (NF-κB) Exploring the effects of Licochalcone A (LCA) on the proliferation, invasion, and drug resistance of glioma cells through signaling pathways.
Methods: Cultivate human glioma cell line U251 in vitro, induce drug-resistant cell line U251/TMZ with Temozolomide (TMZ), and validate the results. Different concentrations of licorice chalcone A were used to treat U251 cells and U251/TMZ cells, and were named as control group, low-dose group, medium-dose group, and high-dose group, respectively.
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