Agricultural Research Organization – Volcani Institute Sionov Lab Agricultural Research Organization – Volcani Institute
Institute of Postharvest & Food Sciences

Some fungi poison our food. Some shrug off the drugs meant to kill them. Often it's the same fungus.

The Sionov Lab studies how mycotoxigenic fungi decide to make toxins, how pathogenic fungi survive the antifungals used against them, and how to find both faster — in the field, in storage, and in the clinic.

Rishon LeZion, Israel · 15 min from Tel Aviv

Aspergillus flavus on agar, day 5. Visible light.

Recent papers

All 56 publications →

Research

Four projects, one organism problem.

Mycotoxins are toxic compounds made by filamentous fungi that colonise fruit, cereals, nuts and spices. Some cause acute poisoning; others drive long-term harm including immune suppression and cancer. The same fungi are increasingly hard to kill, and hard to spot in time. These four projects approach that from different ends.

Illustrated overview of the project.
How the fungus decides to make a toxin — environmental and host signals feed a set of global regulators that switch the biosynthetic cluster on. Illustrative overview.
Project

Mycotoxin regulation

Penicillium expansum · Aspergillus carbonarius · Trichothecium roseum

Toxin genes sit together in biosynthetic clusters, and clusters are expensive to run. The fungus only turns them on under particular conditions — and the host it's sitting in is one of those conditions.

Mycotoxin biosynthesis is governed by cluster-specific regulators, global transcriptional complexes and epigenetic modification. Broad-domain regulators respond to the environment the fungus finds itself in: carbon and nitrogen source, ambient pH, light, oxidative stress. We work on the carbon catabolite repressor CreA, the nitrogen regulator AreA, the pH-responsive factor PacC, the velvet-complex master regulator LaeA, the epigenetic reader SntB and histone demethylase KdmB.

A typical mycotoxin biosynthetic gene cluster carries a backbone enzyme acting on primary metabolites — usually a polyketide synthase or non-ribosomal peptide synthetase — plus tailoring enzymes that decorate the product and alter its bioactivity. Larger clusters add a cluster-specific transcription factor and dedicated transporters for trafficking and secretion.

Our angle is that the host is not a passive substrate. Knocking out regulators in P. expansum changes both patulin output and virulence on Golden Delicious apples, and the apple's own chemistry feeds back onto LaeA and the patulin cluster. We ask which intrinsic and extrinsic factors set toxin production in vitro versus in a colonised fruit — because only the second one matters for food safety.

Illustrated overview of the project.
How a haploid fungus becomes azole-resistant by changing chromosome copy number rather than by mutation. Illustrative overview.
Project

Fungal resistance

Aspergillus flavus · Aspergillus fumigatus · Cryptococcus neoformans

Resistance is typically written into the sequence. We think a fungus can get there by changing how many copies of a chromosome it carries — and change back.

Aneuploidy is an unbalanced chromosome complement: one or more chromosomes present in extra or missing copies. It has long been tied to drug resistance in human pathogenic yeasts — Candida albicans, Cryptococcus neoformans, Candida glabrata, Candida auris — where duplicating a chromosome lets the cell withstand azoles and other stressors without any point mutation at all.

Aspergillus flavus is a filamentous fungus that contaminates major crops with aflatoxins, and it is also the second leading cause of human invasive aspergillosis after A. fumigatus. Azoles are the front-line control in both settings. Resistance in Aspergillus is normally attributed to point mutations in cyp51 orthologues, overexpression of those genes, or efflux pumps lowering the effective drug concentration.

We found an aflatoxigenic A. flavus strain adapting to voriconazole above its MIC through whole and segmental aneuploidy of specific chromosomes — the first experimental evidence of this in a filamentous fungus. Whole-genome sequencing of eight voriconazole-resistant isolates confirmed complete duplication of chromosome 8 in two sequentially isolated clones and a segmental duplication of chromosome 3 in another. That matters because it's fast, it needs no mutation, and it's reversible: repeated transfer on drug-free media returns the clones to their original azole susceptibility. A dosage mechanism, not a sequence one.

Illustrated overview of the project.
From natural sources to a validated antifungal — extraction, screening, and the cellular targets these compounds hit. Illustrative overview.
Project

Natural products as antifungals

Punica granatum · Myrtus communis · Nepenthes khasiana · Dysidea herbacea

Organisms that have been fighting fungi for millions of years are better chemists than we are. The useful question is what happens when you combine their compounds with ours.

The antifungal arsenal is thin and resistance is spreading, so we look for activity in places under real selection pressure: plants that resist fungal attack, carnivorous pitchers that hold digestive fluid without rotting, marine sponges, and agricultural by-products that would otherwise be waste.

Pomegranate peel extract is the clearest case. On its own it suppresses mycotoxigenic fungi; combined with an azole fungicide it acts synergistically, inhibiting both growth and toxin output at doses where neither compound works alone. We've taken the same extract into the ensiling process as a natural additive against fungal and mycotoxin contamination in silage. We've also characterised antifungal naphthoquinones induced in Nepenthes khasiana pitchers, a compound from the sponge Dysidea herbacea, and zinc chloride against A. flavus.

Synergy is the point. A natural product that lets you use less azole, or that closes off a resistance route, is worth more than one that simply kills things in a dish.

Illustrated overview of the project.
From a contaminated sample to an actionable result — the platforms that make mycotoxin detection fast enough to matter. Illustrative overview.
Project

Fungal & mycotoxin detection

Aflatoxin B₁ · Fumonisin B₁ · Ochratoxin A · Patulin · Citrinin

A method that needs two days, a clean bench and an LC-MS/MS is no help to the person standing next to the silo. The measurement has to be where the commodity is.

Mycotoxin contamination is heterogeneous and it moves with the goods. Regulatory limits exist for aflatoxins, ochratoxin A, fumonisins, patulin and the rest, but enforcing them depends on being able to measure quickly, cheaply and at the point the decision is made — at intake, in storage, on the packing line.

With Giorgi Shtenberg's group we develop surface-enhanced Raman scattering platforms on silver-coated porous silicon, including reusable substrates and a microarray that reads aflatoxin B₁, fumonisin B₁ and ochratoxin A together. We've compared aptasensor against immunosensor architectures on the same Ag-pSi substrate for ultrasensitive AFB₁ detection, and built a porous-silicon Fabry-Pérot interferometer for AFB₁ in field crops. In parallel we run chromatographic and mass-spectrometric methods for patulin and citrinin in fruit, and rapid identification of mycotoxigenic fungi and their toxins in stored wheat grain.

Detection and regulation are the same question asked twice. Knowing which conditions switch a cluster on tells you when to look; knowing how to look tells you whether the regulation work was right.

Methods

What we actually do all day

Classic microbiology; analytical chemistry (HPLC, LC-MS/MS); physiological assays; and molecular biology — whole-genome sequencing, comparative transcriptomics, genetic engineering across fungal species, microbiome analysis, and quantitative real-time PCR.

Lab members

The team

Alumni

Where they went next

Publications

Articles in reviewed journals

Every entry links to its DOI. Filter by project or search by author, title or journal.

Contact

Find us

We're at the Institute of Postharvest and Food Sciences, Agricultural Research Organization – Volcani Institute, in the centre of Israel, about fifteen minutes' drive from Tel Aviv.

Group leader
Dr. Edward Sionov
edwardsio@volcani.agri.gov.il
Office 03-9683693
Mobile 050-6220693
Lab
03-9683522
03-9683653
Address
68 HaMaccabim Road
Rishon LeZion 7505101
Israel
Join us

We're glad to hear from people who want to work on this.

We take M.Sc. and Ph.D. students and host postdocs and visiting researchers. You don't need to wait for an advertised position — if the work below sounds like yours, write to Edward with a CV and a paragraph on what you'd want to do here.

  • Fungal genomics and comparative transcriptomics
  • Chromosome-level variation and drug resistance
  • Analytical chemistry of mycotoxins (HPLC, LC-MS/MS)
  • Biosensors and rapid detection platforms
  • Genetic engineering of filamentous fungi
  • Food-safety microbiology and postharvest pathology
Write to Edward