Genetic switch between unicellularity and multicellularity in marine yeasts
Article Date: 07 January 2026
Article URL: https://www.nature.com/articles/s41586-025-09881-4
Article Title: Genetic switch between unicellularity and multicellularity in marine yeasts
Article Image: (no image provided)
Summary
Kurita et al. report mechanistic and genetic control of a reversible switch between unicellular and multicellular growth in marine-derived yeasts (notably Hortaea werneckii). Using genome sequencing, RNA-seq, mutant screens and live imaging, the authors identify key regulators—principally the Myb1 transcription factor—and show that environmental cues (nutrients and sponge-conditioned medium) and regulated proteasome-dependent degradation of Myb1 drive transitions between budding (unicellular) and septation-based multicellular forms. The phenomenon is shown across ecotypes and related species, with multiple genes (veA, flo8, cip2, flbA/D, orb6, etc.) influencing the balance.
Key Points
- Myb1 acts as a central regulator: high Myb1 levels promote unicellular budding, while rapid Myb1 degradation triggers multicellular septation.
- Proteasome activity controls Myb1 abundance — proteasome inhibition prevents Myb1 loss and suppresses multicellularity induction.
- Nutrient cues (notably external polypeptone/amino acids) and sponge-conditioned medium strongly bias H. werneckii towards multicellular growth, demonstrating environmental control of the switch.
- Mutant screens identified multicellular-prone and unicellular-prone alleles (veA, flo8, myb1, cip2, flbA/D, orb6, ptaB among others), revealing a regulatory network connecting transcription factors, signalling and cell-cycle/polarity pathways.
- The switch is plastic across ecotypes (NU195 vs NU219) and observed in related fungi (N. pruni, Cladosporium sp.), suggesting conserved or repeatedly co-opted mechanisms in fungal lineages.
- Approaches used: draft genome assemblies, RNA-seq differential expression (165 DEGs), targeted gene deletions, auxin-inducible degron (mAID) to force Myb1 degradation, time-lapse imaging and biochemical inhibition (bortezomib).
Content summary
The authors combined genomic resources (draft assemblies, raw reads and RNA-seq) with genetic manipulation and high-resolution imaging to dissect facultative multicellularity in marine yeasts. They show that H. werneckii can switch growth modes depending on cell density, nutrient composition and cues from a sponge-conditioned medium. Mutagenesis and selection screens produced strains biased to either multicellular or unicellular growth. Key genes were knocked out or manipulated: deletion of myb1 and several other regulators produced dominant multicellular phenotypes, while cip2 and others favoured budding.
Myb1 protein levels fall rapidly when cells are diluted or exposed to permissive conditions for multicellularity; forced degradation of Myb1 via an auxin-inducible degron immediately induces multicellularisation. Conversely, overexpression of Myb1 sustains unicellular growth. Proteasome inhibition (bortezomib) blocks Myb1 reduction and suppresses the switch, implicating ubiquitin–proteasome control of the decision point. Transcriptome comparisons between multicellular and unicellular states revealed 165 differentially expressed genes and enriched GO terms pointing to developmental and stress-response modules.
Experiments extend to different ecotypes: NU219 (sponge-derived) is more prone to multicellularity than NU195, and related species (Neodothiora/N. pruni and Cladosporium) retain aspects of facultative multicellularity and share functional requirements for certain regulators (for example Myb1 function in conidiation in Cladosporium). Methods include protoplast-based transformation, homologous recombination, RNA-seq, and extensive time-lapse imaging (supplementary videos document nutrient responses, mutant behaviours and dynamics of Myb1).
Context and relevance
Punchy take: this paper gives a clear, experimentally tractable example of an environmentally responsive developmental switch between uni- and multicellular lifestyles in fungi. That matters because it ties cellular plasticity to specific molecular players and proteostasis control — a tangible mechanism by which developmental polyphenism and possibly early steps of multicellular evolution might arise or be regulated. The work sits at the intersection of evolutionary biology, cell polarity/cycle research and fungal genetics, and provides a model system for testing how selection and environment interact to produce multicellular traits.
Broader implications include insights into how stress- or environment-responsive genes can be co-opted into developmental roles, and how relatively simple regulatory changes (protein degradation, transcriptional reprogramming) can flip major life-history states. For researchers studying the origins of multicellularity, phenotypic plasticity or fungal development, the paper offers molecular candidates, genetic tools and live-cell datasets to build on.
Why should I read this
Short and informal: fancy a neat molecular story about how a yeast decides to be single-celled or join a club? This paper nails a switch you can see under the microscope, names the main player (Myb1) and shows it’s controlled by the proteasome and environmental signals — plus there are mutants and videos. If you want a clean, testable link between environment, protein turnover and social behaviour in microbes, this is worth your five minutes (or a deeper read if you work on evolution or fungi).