Special Issue "Molecular Biology and Genomic Strategies to Mitigate the Effects of Mycotoxins"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Mycotoxins".

Deadline for manuscript submissions: closed (30 November 2019).

Special Issue Editors

Prof. Dr. Kent M. Reed
E-Mail Website
Guest Editor
Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108, USA
Interests: biotechnology; genomics; evolutionary biology; molecular biology
Prof. Dr. Roger A. Coulombe, Jr.
E-Mail Website
Guest Editor
Department of Animal, Dairy and Veterinary Sciences, College of Agriculture and Applied Sciences, Utah State University, Logan, UT 84322, USA
Tel. 435,797,1598
Interests: molecular toxicology; functional genomics of disease; food safety; dietary carcinogens; mechanisms of carcinogenesis and chemoprevention

Special Issue Information

Dear Colleagues,

Mycotoxins are secondary metabolites produced by ubiquitous fungi that are toxic to humans, animals, and plants. The majority of species in the genera Aspergillus, Penicillium, and Fusarium grow on food and feeds, posing a risk to human and animal health, and carry through to food products. The extent of mycotoxin contamination is exacerbated by increasingly unfavorable environmental conditions, including temperature and humidity changes resulting from climate change. Although much research has been dedicated to identifying means to mitigate the effects of mycotoxin exposure, there is an increasing need to identify and understand the genetic basis of resistant phenotypes. Phenotypes that can either be applied to animal populations through genetic selection or engineered to enhance mycotoxin resistance will be of increased value and necessity.

The focus of this Special Issue of Toxins is the application of molecular toxicology, molecular biology, and genomic tools, including high throughput assays, to understand the genetic basis for variation in response to environmental mycotoxins. The ultimate aim of such studies is the identification of resistant genomes to reduce the impact of mycotoxins linked to human and animal disease and toxicity.

Prof. Dr. Kent M. Reed
Prof. Dr. Roger A. Coulombe, Jr.
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mycotoxins
  • molecular toxicology
  • genomics
  • bioinformatics
  • genetics

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Open AccessArticle
Comparative Sequence Analysis of TRI1 of Fusarium
Toxins 2019, 11(12), 689; https://doi.org/10.3390/toxins11120689 - 23 Nov 2019
Abstract
Trichothecene mycotoxins are a class of secondary metabolites produced by multiple genera of fungi, including certain plant pathogenic Fusarium species. Functional variation in the TRI1 gene produces a novel Type A trichothecene called NX-2 in strains of F. graminearum. Using a bioinformatics [...] Read more.
Trichothecene mycotoxins are a class of secondary metabolites produced by multiple genera of fungi, including certain plant pathogenic Fusarium species. Functional variation in the TRI1 gene produces a novel Type A trichothecene called NX-2 in strains of F. graminearum. Using a bioinformatics approach, a systematic analysis of 52 translated TRI1 sequences of Fusarium species, including five F. graminearum NX-2 producers and four F. graminearum non-NX-2 producers, was conducted to explain the functional difference of TRI1p of FGNX-2. An assessment of several signature motifs of fungal P450s revealed amino acid substitutions in addition to the post-translational N-X-S/T sequons motif, which is indicative of N-linked glycosylation of this TRI1-encoded protein characteristic of NX-2 producers. There was evidence of selection bias, where TRI1 gene sequences were found to be under positive selection and, therefore, under functional constraints. The cumulative amino acid changes in the TRI1p sequences were reflected in the phylogenetic analyses which revealed species-specific clustering with a distinct separation of FGNX-2 from FG-non-NX-2 producers with high bootstrap support. Together, our findings provide insight into the amino acid sequence features responsible for the functional diversification of this TRI1p. Full article
Show Figures

Figure 1

Open AccessArticle
Towards Managing and Controlling Aflatoxin Producers Within Aspergillus Species in Infested Rice Grains Collected from Local Markets in Kenya
Toxins 2019, 11(9), 544; https://doi.org/10.3390/toxins11090544 - 19 Sep 2019
Abstract
Rice grains can be attacked by a range of pathogens, including Aspergillus species, which can cause the accumulation of aflatoxins and represent a serious threat to the consumers. Aflatoxins are secondary metabolites synthesized by Aspergillus species and naturally occur in various foodstuffs. In [...] Read more.
Rice grains can be attacked by a range of pathogens, including Aspergillus species, which can cause the accumulation of aflatoxins and represent a serious threat to the consumers. Aflatoxins are secondary metabolites synthesized by Aspergillus species and naturally occur in various foodstuffs. In this study, we sought to analyze the prevalence of aflatoxin-producing Aspergillus spp. in rice grains currently sold in Kenyan local markets. We analyzed a total of 98 samples randomly collected and primarily analyzed to observe moisture content and fungal growth. We then isolated Aspergillus species, characterized them morphologically and using the Internal transcribed spacer (ITS) primers. Finally, we screened them for aflatoxin-producing isolates targeting Norsolorinic Acid (nor-1) and Versicolorin (ver-1) specific genes involved in aflatoxin biosynthesis. We observed that all tested samples were contaminated. The highest prevalence of Aspergillus species and aflatoxigenic fungal species, had values of 66% and 36.4% for nor-1 and ver-1, respectively. In total, 66% of all isolates were confirmed to be aflatoxin producers. The occurrence of high contamination levels of Aspergillus species points to the possibility of production of aflatoxins in rice grains. This work provides a baseline for future studies on the occurrence of mycotoxigenic fungal species in rice grains being sold in local markets and strategies to control these aflatoxigenic strains at pre- and post-harvest levels. Full article
Show Figures

Figure 1

Open AccessArticle
Altered Gene Response to Aflatoxin B1 in the Spleens of Susceptible and Resistant Turkeys
Toxins 2019, 11(5), 242; https://doi.org/10.3390/toxins11050242 - 28 Apr 2019
Abstract
Susceptibility and/or resistance to aflatoxin B1 (AFB1) is a threshold trait governed principally by glutathione S transferase (GST)-mediated detoxification. In poultry, domesticated turkeys are highly sensitive to AFB1, most likely due to dysfunction in hepatic GSTs. In contrast, [...] Read more.
Susceptibility and/or resistance to aflatoxin B1 (AFB1) is a threshold trait governed principally by glutathione S transferase (GST)-mediated detoxification. In poultry, domesticated turkeys are highly sensitive to AFB1, most likely due to dysfunction in hepatic GSTs. In contrast, wild turkeys are comparatively resistant to aflatoxicosis due to the presence of functional hepatic GSTAs and other possible physiological and immunological interactions. The underlying genetic basis for the disparate GST function in turkeys is unknown as are the broader molecular interactions that control the systemic response. This study quantifies the effects of dietary AFB1 on gene expression in the turkey spleen, specifically contrasting genetically distinct domesticated (DT, susceptible) and Eastern wild (EW, resistant) birds. Male turkey poults were subjected to a short-term AFB1 treatment protocol with feed supplemented with 320 ppb AFB1 beginning on day 15 of age and continuing for 14 days. Spleen tissues were harvested and subjected to deep RNA sequencing and transcriptome analysis. Analysis of differential gene expression found the effects of AFB1 treatment on the spleen transcriptomes considerably more prominent in the DT birds compared to EW. However, expression of the differentially expressed genes (DEGs) was directionally biased, with the majority showing higher expression in EW (i.e., down-regulation in DT). Significantly altered pathways included FXR/RXR and LXR/RXR activation, coagulation system, prothrombin activation, acute phase response, and atherosclerosis signaling. Differential extra-hepatic expression of acute phase protein genes was confirmed by quantitative real time PCR (qRT-PCR) in the original experiment and additional turkey lines. Results demonstrate that wild turkeys possess a capacity to more effectively respond to AFB1 exposure. Full article
Show Figures

Figure 1

Back to TopTop