Fungi have repeatedly delivered transformative advances across industries, from medicine to food to materials, yet these breakthroughs have emerged from a narrow base of organisms and well-studied systems. Although mycology has taken a big leap forward in the past decades because of advances in genomics, multi-omics, engineering, phenotyping and environmental monitoring, much fungal diversity remains taxonomically and functionally under-characterised, and many sustainability-relevant innovations remain limited by lack of investment, sparse infrastructure, and fragmented governance. We now have technologies that make previously inaccessible fungal questions tractable, which can help unlock the next generation of fungal breakthroughs. Informed by a workshop held in December 2025 that convened 20 leading experts across fungal disciplines, here we lay out key bottlenecks to fungal research and innovation through three lenses: functional mycology, human and institutional capacity, and governance. We identify selected sustainability-relevant fungal frontiers and use these to surface the recurrent gaps that cut across domains. We propose four elements of coordinated action across research and development, governance, and advocacy that could contribute to unlocking the full potential of fungi for sustainability transitions.
Esca remains one of the most conceptually challenging disease syndromes of grapevine because it cannot be reduced to a single pathogen, lesion type or external phenotype. Foliar symptoms are erratic, internal wood damage is heterogeneous, and fungi associated with the syndrome may persist in asymptomatic vines. Much of this difficulty stems from treating esca-associated fungi as functionally equivalent, even though they occupy different niches and contribute differently to disease development. Here, we revisit grapevine esca through a fungal-biology-centred framework focused on Phaeomoniella chlamydospora, Phaeoacremonium minimumand white-rot basidiomycetes, especially Fomitiporia mediterranea. We argue that the esca pathosystem is best understood as the interaction between two biologically connected but non-equivalent fungal layers: a pioneer vascular phase and a later white-rot phase. Within this perspective, Petri disease and esca proper are interpreted as stages along a continuous host-fungus trajectory shaped by colonization strategy, tissue occupation, decay biology and pathobiome context. This distinction clarifies why host phenotypes are so difficult to interpret. Current evidence supports partially independent layers of host response, including resistance to pioneer colonization, tolerance to hydraulic dysfunction, resistance to wood decay and resilience under chronic infection. We therefore propose that “esca resistance” should be interpreted not as a unitary host trait, but as a multidimensional consequence of fungal functional differentiation, host physiology and environmental modulation.
The genus Sarocladium (order Hypocreales) comprises filamentous fungi engaging in diverse interactions with plants. While many species of this genus function as endophytes, some are also capable of causing diseases such as the infamous rice sheath rot. In this review, we synthesize current knowledge on these contrasting plant-associated lifestyles. Metabarcoding studies indicate that Sarocladium species are widespread, occurring predominantly in soil, air, and plant samples from vegetated biomes. These fungi behave as free-living saprobes and endosymbionts of plants, primarily—though not exclusively—of poaceous grasses. Notably, several of these species share biological characteristics with Class 2 endophytes, a diverse polyphyletic group with extensive transmission and colonization abilities, often associated with stress tolerance. We argue that necrotrophic traits, which appear largely opportunistic within Sarocladium, have sporadically emerged in several endophytic (sub)species; their origins and manifestation are examined herein. Finally, we propose future research avenues focusing on neglected metabolomics, genomics, and ecological aspects of the genus.
Quiescence, a reversible and non-proliferative state, is a critical cellular response to stress and unfavorable conditions, allowing cells to temporarily exit the cell cycle. This state plays a vital role in various biological processes, including tissue repair and immune responses. However, disruptions in the balance of quiescence can lead to health issues such as aging and cancer recurrence. Consequently, a profound understanding of the molecular underpinnings of quiescence is imperative for the development of targeted therapeutics to address disorders arising from quiescence dysregulation. The entry and exit of quiescence lead to extensive changes in gene expression, with studies emphasizing the importance of chromatin mechanisms. In this article, we review the current literature on chromatin remodeling and RNAi-mediated gene silencing during the quiescence in fission yeast Schizosaccharomyces pombe (S. pombe), which can enter quiescence via depletion of nutrients such as glucose and nitrogen. Specifically, our recent findings have revealed that Coilin and Cajal bodies play critical roles in promoting mRNA splicing and repressing RNA polymerase I transcription during quiescence, offering new insights into quiescence maintenance and exit. Yet, the mechanisms of chromatin and RNA-mediated regulation during quiescence remain poorly defined. Given its contributions and advantages in studying cellular quiescence and chromatin, S. pombe remains an excellent model organism for further research.
Fungi represent a diverse source of bioactive compounds with the potential to influence genomic stability in both harmful and beneficial ways. Some species produce metabolites capable of inducing DNA damage through direct interaction with genetic material or via metabolic activation, while others yield compounds that may protect against oxidative stress and mutagenesis. The scientific literature on this topic, however, contains notable contradictions, with discrepancies often stemming from differences in methodology, experimental models, and data interpretation. This review critically examines current evidence on the genotoxic and protective effects of fungi, while also addressing the challenges posed by inaccuracies and inconsistencies in published studies. Overall, fungal effects on genomic stability depend strongly on the chemical composition of fungal materials, the concentration and bioavailability of their constituents, and the experimental context. The reviewed evidence indicates that fungal compounds can exert both genotoxic and genoprotective effects, highlighting the need to distinguish direct genotoxicity from secondary DNA damage and antioxidant-mediated protection.
