Evidence map›Paper›PMID 37955405›Full record

ArticleACS infectious diseases2023

Potency of CRISPR-Cas Antifungals Is Enhanced by Cotargeting DNA Repair and Growth Regulatory Machinery at the Genetic Level.

Brian J Mendoza, Xianliang Zheng, Jared C Clements, Christopher Cotter, Cong T Trinh

Open access · greenAbstract read
In one paragraph

Article in ACS infectious diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Brian J MendozaDepartment of Chemical and Biomolecular Engineering, University of Tennessee, Knoxville, Tennessee 37996, United States.
Xianliang ZhengDepartment of Chemical and Biomolecular Engineering, University of Tennessee, Knoxville, Tennessee 37996, United States.
Jared C ClementsDepartment of Chemical and Biomolecular Engineering, University of Tennessee, Knoxville, Tennessee 37996, United States.
Christopher CotterDepartment of Chemical and Biomolecular Engineering, University of Tennessee, Knoxville, Tennessee 37996, United States.
Cong T TrinhDepartment of Chemical and Biomolecular Engineering, University of Tennessee, Knoxville, Tennessee 37996, United States.ORCID 0000-0002-8362-725X
University of Tennessee at Knoxville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The emergence of virulent, resistant, and rapidly evolving fungal pathogens poses a significant threat to public health, agriculture, and the environment. Targeting cellular processes with standard small-molecule intervention may be effective but requires long development times and is prone to antibiotic resistance. To overcome the current limitations of antibiotic development and treatment, this study harnesses CRISPR-Cas systems as antifungals by capitalizing on their adaptability, specificity, and efficiency in target design. The conventional design of CRISPR-Cas antimicrobials, based on induction of DNA double-strand breaks (DSBs), is potentially less effective in fungi due to robust eukaryotic DNA repair machinery. Here, we report a novel design principle to formulate more effective CRISPR-Cas antifungals by cotargeting essential genes with DNA repair defensive genes that remove the fungi's ability to repair the DSB sites of essential genes. By evaluating this design on the model fungus

Indexed as

Antifungal AgentsCRISPR-Cas SystemsAnti-Bacterial AgentsDNA RepairRNA, Guide, CRISPR-Cas SystemsSaccharomyces cerevisiaeAnti-Bacterial AgentsAntifungal AgentsRNA, Guide, CRISPR-Cas Systemsantibiotic resistanceCas enzymesCRISPRCRISPR-Cas antifungaldefensive genesessential and defensive gene cotargetingessential geneshomologous recombination (HR)nonhomologous end joining (NHEJ)Saccharomyces cerevisiae

Identifiers

PMID37955405
PMCPMC10714396
OpenAlexW4388639006

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.