Biology subjects

Di Pietro, A.

Publications and source records attributed to Di Pietro, A..

At least 19 recordsLinked to original sources

bioRxiv2026

Killer meiotic driver prevents chromosome loss and enhances fitness in a fungal pathogen

Fungal pathogens often carry dispensable chromosomes (DCs) that confer a selective advantage in adverse environments or during host infection but can be spontaneously lost under non-selective conditions. How DCs are maintained in evolving populations remains poorly understood. Here we show that a meiotic driver known as Spore Killer (spok), located on a giant Starship transposon, limits spontaneous loss of a conserved DC in the cross-kingdom pathogen Fusarium oxysporum. Transfer of a functional spok gene, but not of a killing-deficient mutant allele, to a mitotically unstable DC significantly reduced its loss rate, while spok deletion from a stably maintained DC increased loss frequency. Competition experiments between isogenic strains carrying a functional or a killing-deficient spok allele revealed a dramatic fitness gain conferred by Spok killing activity, which required transmission by hyphal fusion. Thus, spoks and their Starship carriers benefit fungal hosts by preventing DC loss and preserving long-term metabolic and pathogenic plasticity.

microbiology↗

bioRxiv2026

Embedding wear assessment in musculoskeletal simulation: A proof-of-concept application to total hip arthroplasty

Predicting wear in artificial joints requires integrating joint dynamics, contact mechanics and progressive surface evolution, yet these processes are often treated separately. In total hip arthroplasty (THA), finite-element approaches remain the reference standard, but they are computationally demanding and usually rely on boundary conditions from independent musculoskeletal (MSK) models, hindering consistent coupling and feedback between wear progression and movement dynamics. As a single-subject proof of concept, we present a computational framework that embeds wear estimation within forward MSK simulations through OpenSim-MATLAB integration. Contact variables are computed using an elastic-foundation formulation, and wear is updated through the Archard law, enabling cyclic prediction of contact mechanics and surface evolution within a single workflow at practical computational cost. The framework was evaluated in one subject with right THA during five activities of daily living and numerically benchmarked against finite-element simulations. A long-term walking analysis of 4 million cycles was also performed to assess geometry updating. Across tasks, peak contact pressures remained within 7% of finite-element predictions. Linear wear depth and volumetric loss showed maximum deviations of 16% and 13%, respectively. Accounting for progressive geometry changes yielded a maximum wear depth about 31% lower than linear extrapolation. These preliminary results support the framework's computational feasibility and numerical consistency for the tested case; nevertheless, multi-subject evaluation is required before broader predictive or clinical use.

bioengineering↗

bioRxiv2026

A near-complete genome assembly of the Fusarium oxysporum keratitis isolate MRL8996

Fusarium oxysporum MRL8996 is a fungal strain isolated from a severe case of contact lens-associated keratitis. Here we report a near-complete genome assembly of this isolate using a hybrid Nanopore and Hi-C scaffolding approach. The assembly resolves the genome into 16 distinct chromosomes, including 11 core and 5 lineage-specific chromosomes. This high-quality reference genome provides an unprecedented tool for investigating the large-scale structural variations and evolutionary mechanisms driving adaptation in this highly versatile fungal lineage.

genomics↗

bioRxiv2026

Mycol: A user-friendly app for automating analysis of microscopy images

Microscopy image analysis is central to modern biology, yet many available platforms remain inaccessible to non-specialist users because they require advanced technical expertise, code-based workflows, extensive setup, or paid access. This creates a barrier for researchers who need reliable and fast image quantification but lack dedicated computational support. Here, we introduce Mycol, an open-source, machine-learning-assisted image analysis platform designed to be accessible and run on standard laptops with minimal setup. Mycol supports end-to-end workflows in which users annotate microscopy images, perform human-in-the-loop fine-tuning of machine learning models for automated segmentation and classification, deploy machine learning models, quality control predictions and quantitatively compare morphological and class frequency descriptors through a single intuitive interface. By combining machine-learning analysis with efficient quality control by humans, Mycol makes rapid and high-quality image quantification available to biologists without requiring specialist training. We demonstrate the utility of Mycol in diverse workflows using two economically important organisms, the crop pathogen (Fusarium oxysporum) and the blue mussel (Mytilus edulis). Through Mycol, curated training sets were generated and high quality segmentation and classification models were obtained in each case. Deploying these models through Mycol decreased the time requirements and increased traceability of established cell counting workflows and facilitated a quantitative comparison of morphological parameters that reveals new patterns in early M. edulis larval development.

bioinformatics↗

bioRxiv2026

A chromosome-level assembly of the Fusarium oxysporum biocontrol strain FO12

Fusarium oxysporum FO12 was originally isolated from cork oak (Quercus suber L.) and has been characterised as a highly effective biological control agent of wilt diseases on different crops. FO12 endophytically colonises roots and basal stems of plants, reducing the establishment of the soil-borne pathogen Verticillium dahliae and triggering plant defence-related genes. Here, we report a chromosome-level genome assembly of FO12 using Nanopore and Hi-C data. The 57.60 Mb assembly comprises 14 chromosome-scale scaffolds with centromeres resolved and telomeric repeats detected at 4 of 28 chromosome ends. This high-quality reference genome provides a valuable resource for further research into the use of FO12 in agriculture as a biocontrol agent.

genomics↗

bioRxiv2025

OpenGRF: Predicting Ground Reaction Forces and Moments During Daily Living Activities in OpenSim

Background and ObjectivesGround reaction forces and moments (GRF&Ms), typically measured using force plates, are key inputs for musculoskeletal simulations. OpenSim currently lacks a tool to predict GRF&Ms directly from kinematics. This study presents OpenGRF, an OpenSim-based tool designed to estimate GRF&Ms and the centre of pressure (CoP) from joint kinematic data and validates its performance against force plate recordings. MethodsThe proposed methodology integrates calibrated foot-ground contact probes with an optimization framework based on computed muscle control, while CoP is computed accounting for both kinematic and dynamic contributions. For validation, a scaled FullBodyModel (37-DoF without muscles) was created for seven healthy adults performing six trials each of level walking, stair ascent, and stair descent, for a total of 126 marker-based trials. GRF&Ms predictions were compared to reference force plate data using normalized RMSE (nRMSE), Pearson correlation coefficients ({rho}), CoP error, and Statistical Parametric Mapping (SPM) ResultsResults showed high accuracy for vertical GRF (nRMSE [≤]1.5%, {rho} [≥]0.94), particularly during level walking, and good accuracy for anterior-posterior GRF (nRMSE 4.4-6.1%, {rho} = 0.81-0.91). Medio-lateral GRF was less reliable, especially in stair tasks (nRMSE up to 11.2%, {rho} down to 0.48). Free moments were the most challenging quantity to predict across all tasks (nRMSE up to 28%). In contrast, ankle moments were predicted with high fidelity (nRMSE {approx}1.7%, {rho} {approx}0.98). Median CoP errors were 21-23 mm, with largest discrepancies during double support. ConclusionsOpenGRF enables physics-consistent estimation of GRF&Ms and CoP directly from kinematics, achieving the highest accuracy for vertical GRFs and predicting ankle moments that closely match those obtained from force plate measurements.

bioengineering↗

bioRxiv2025

Transcriptional plasticity of fast core chromosomes governs establishment of a fungal pathogen on evolutionarily distant plant lineages

The Fusarium oxysporum (Fo) species complex encompasses a diverse range of filamentous plant pathogens, some of which provoke systemic infections in angiosperms, leading to vascular wilt disease. Current understanding of the Fo pathogenicity mechanisms is primarily centered on vascular plants, where individual isolates of Fo exhibit contrasting lifestyles across the endophyte-pathogen continuum on different host species. Although, Fo isolates were recently shown to cause disease on the non-vascular liverwort Marchantia polymorpha (Mp), the transcriptional control of Fo effectors during infection of this bryophytic host is largely unknown. Here, we took a comparative transcriptomic approach to ask how different Fo isolates with contrasting interaction outcomes on angiosperms (pathogenic versus endophytic) adapt to a distantly related plant lineage lacking xylem. We found that the core effector complement encoded on genomic regions shared across all Fo isolates are actively transcribed in Mp, whereas effectors encoded on lineage-specific (LS) genomic regions that contribute towards host-specific pathogenicity in angiosperms are not. Moreover, we observed enhanced transcriptional activation of effector clusters located on the three highly syntenic fast core chromosomes during growth on Mp, as well as divergent lineages and lifestyles, suggesting a conserved role in plant associations. Loss of a compatibility-associated effector encoded in a core effector cluster led to misregulation of other effectors in core clusters. Our findings reveal an unexpected role of fast core chromosomes in determining compatibility of Fo across a broad spectrum of plant lineages and establishes evolutionarily conserved gene networks essential for fungus-plant associations.

plant biology↗

bioRxiv2025

Transposons and accessory genes drive adaptation in a clonally evolving fungal pathogen

Genomes of clonally reproducing fungal pathogens are often compartmentalized into conserved core and lineage-specific accessory regions (ARs), enriched in transposable elements (TEs). ARs and TEs are thought to promote pathogen adaptation, but direct experimental evidence is sparse. Using an evolve and re-sequence approach, we found that serial passaging of the cross-kingdom fungal pathogen Fusarium oxysporum through tomato plants or axenic media rapidly increased fitness under the selection condition. TE insertions were the predominant type of mutations in the evolved lines, with a single non-autonomous hAT-type TE accounting for 63% of total events detected. TEs inserted preferentially at sites of histone H3 lysine 27 trimethylation, a hallmark of ARs. Recurrent evolutionary trajectories during plate adaptation led to increased proliferation concomitant with reduced virulence. Unexpectedly, adaptive mutations in accessory genes strongly impacted core functions such as growth, development, quorum sensing or virulence. Thus, TEs and ARs drive rapid adaptation in this important fungal pathogen.

microbiology↗

bioRxiv2024

Extensive intrachromosomal duplications in a virulence-associated fungal accessory chromosome

Filamentous fungi have evolved compartmentalized genomes consisting of conserved core regions and dynamic accessory regions, which aid the adaptation to changing environments including the interaction with host organisms. In the Fusarium oxysporum species complex, accessory regions play an important role during infection and it has been reported that these regions undergo extensive duplications, however, it is currently unknown how such duplications shape accessory regions. Moreover, the function of accessory regions apart from encoding virulence effectors is not completely understood. Here we determined the karyotype of F. oxysporum Tropical Race 4 (TR4), which causes the ongoing pandemic of Fusarium wilt of banana (FWB). We show that the single accessory chromosome of TR4 isolate II5 has undergone extensive intrachromosomal duplications, resulting in triplication of the chromosome size compared to other closely related TR4 strains. By obtaining mutant strains that have lost the accessory chromosome, we demonstrate that this chromosome is dispensable for vegetative growth but is required for full virulence on banana. Lastly, we found that the loss of chromosome 12 co-occurs with structural rearrangements of core chromosomes, which are generally co-linear between members of the F. oxysporum species complex. Together, our results provide new insights into the chromosome dynamics of the banana infecting TR4 lineage of the F. oxysporum species complex. SignificanceFusarium oxysporum is a major fungal plant pathogen that causes vascular wilt disease on a wide variety of agronomically important crops. A current epidemic of Fusarium wilt of banana (FWB), caused by tropical race 4 (TR4), poses a major threat to global banana production and threatens food security in tropical and subtropical regions where banana is an important staple crop. Controlling TR4 requires a better understanding of the molecular mechanisms underlying pathogenicity, including the evolution of pathogenicity-related accessory regions. Here we demonstrate that intrachromosomal duplications are a key mechanism of accessory chromosome evolution in the F. oxysporum species complex. We identified a single accessory chromosome and show that TR4 mutants that lost this accessory chromosome display significantly reduced virulence on banana plants. Our results provide insight into the evolution of accessory chromosomes in the F. oxysporum species complex, underscore their importance in pathogenicity, and provide new clues for the development of resistant banana plants.

microbiology↗

bioRxiv2024

Copper acquisition is essential for plant colonization and virulence in a root-infecting vascular wilt fungus

Phytopathogenic fungi provoke devastating agricultural losses and are difficult to control. How fungal pathogens adapt to the plant environment to cause disease and complete their life cycle on the host remains poorly understood. Here we show that efficient acquisition of copper, mediated by the transcriptional regulator Mac1, is crucial for plant colonization and virulence in Fusarium oxysporum, a soilborne ascomycete that causes vascular wilt on more than 150 different crops. RNA-seq and ChIP-seq establish a direct role of Mac1 in activation of copper deficiency response genes, many of which are induced during plant infection. Loss of Mac1 impairs growth of F. oxysporum under copper-limiting condition as well as vascular colonization and virulence on tomato plants. Importantly, Mac1-independent overexpression of a copper reductase and a copper transporter restores growth under copper limitation and virulence in the mac1 null mutant background. These findings establish a key role for copper acquisition in fungal pathogenicity on plants and reveal new ways to protect crops from phytopathogens.

genetics↗

bioRxiv2022

Cytosolic pH controls fungal MAPK signaling and pathogenicity

In fungi, ambient pH acts as a key regulator of development and virulence. The vascular wilt pathogen Fusarium oxysporum uses host alkalinization to promote infection of plant hosts through activation of the invasive growth mitogen-activated protein kinase (MAPK) Fmk1. The molecular events underlying pH-driven MAPK regulation are unknown. Using the ratiometric GFP-based pH sensor pHluorin, we find that both F. oxysporum and Saccharomyces cerevisiae respond to extracellular alkalinization or acidification with a transitory shift in cytosolic pH (pHc) and rapid changes in phosphorylation levels of the three fungal MAPKs Fmk1, Mpk1/Slt2 (cell wall integrity) and Hog1 (hyperosmotic stress). Pharmacological inhibition of the essential plasma membrane H+-ATPase Pma1, which leads to pHc acidification, is sufficient to trigger reprogramming of MAPK phosphorylation even in the absence of an extracellular pH shift. Screening of a subset of S. cerevisiae mutants identified the sphingolipid-regulated AGC kinase Ypk1/2 as a key upstream component of pHc-modulated MAPK responses. We further show that acidification of pHc in F. oxysporum leads to an increase of the long chain base (LCB) sphingolipid dihydrosphingosine (dhSph) and that exogenous addition of dhSph activates Mpk1 phosphorylation. Our results reveal a pivotal role of pHc in the regulation of MAPK signaling and suggest new ways to control fungal growth and pathogenicity.

microbiology↗

bioRxiv2022

Constitutive activation of TORC1 signaling attenuates virulence in the cross-kingdom fungal pathogen Fusarium oxysporum

The filamentous fungus Fusarium oxysporum causes vascular wilt disease in a wide range of plant species and opportunistic infections in humans. Previous work suggested that invasive growth in this pathogen is controlled by environmental cues such as pH and nutrient status. Here we investigated the role of Target Of Rapamycin Complex 1 (TORC1), a global regulator of eukaryotic cell growth and development. Inactivation of the negative regulator Tuberous Sclerosis Complex 2 (Tsc2), but not constitutive activation of the positive regulator Gtr1, in F. oxysporum resulted in inappropriate activation of TORC1 signaling under nutrient limiting conditions. The tsc2{Delta} mutants showed reduced colony growth on minimal medium with different nitrogen sources and increased sensitivity to cell wall or high temperature stress. Furthermore, these mutants were impaired in invasive hyphal growth across cellophane membranes and exhibited a marked decrease in virulence, both on tomato plants and on the invertebrate animal host Galleria mellonella. Importantly, invasive hyphal growth in tsc2{Delta} strains was rescued by rapamycin-mediated inhibition of TORC1. Collectively, these results reveal a key role of TORC1 signaling in development and pathogenicity of F. oxysporum and suggest new potential targets for controlling fungal infections. AUTHOR SUMMARYFilamentous fungal pathogens cause devastating losses in agriculture and lethal infections in humans. A prerequisite of fungal infection is invasive hyphal growth, a process that is exquisitely controlled by environmental cues including nutrients and host signals. Here we examined the role of TOR complex 1 (TORC1), a conserved pathway that regulates cell growth in response to nutrient status. We show that deregulation of TORC1 signaling impairs pathogenicity in Fusarium oxysporum, a cross-kingdom fungal pathogen that attacks more than 150 different crops as well as immunocompromised humans. Inactivation of Tsc2, a negative regulator of TORC1, led to constitutive TORC1 activation, reduced growth under nutrient-limiting conditions and increased sensitivity to cell wall stress. Importantly, tsc2{Delta} mutants were impaired in invasive hyphal growth and in virulence on plant and animal hosts. Our results support a conserved role of TORC1 as a negative regulator of pathogenicity-related functions and reveal new leads for antifungal drug discovery.

genetics↗

bioRxiv2022

Components of TOR and MAP kinase signaling control chemotropism and pathogenicity in a fungal pathogen

Filamentous fungi can sense useful resources and hazards in their environment and direct growth of their hyphae accordingly. Chemotropism ensures access to nutrients, contact with other individuals (e.g., for mating), and interaction with hosts in the case of pathogens. Previous studies have revealed a complex chemotropic sensing landscape during host-pathogen interactions, but the underlying molecular machinery remains poorly characterized. Here we studied mechanisms controlling directed hyphal growth of the important plant-pathogenic fungus Verticillium dahliae towards different chemoattractants. We found that the homologs of the Rag GTPase Gtr1 and the GTPase-activating protein Tsc2, an activator and a repressor of the TOR kinase respectively, play important roles in hyphal chemotropism towards nutrients, plant-derived signals, and heterologous -pheromone of Fusarium oxysporum. Furthermore, important roles of these regulators were identified in fungal development and pathogenicity. We also found that the mitogen-activated protein kinase (MAPK) Fus3 is required for chemotropism towards nutrients, while the G protein-coupled receptor (GPCR) Ste2 and the MAPK Slt2 control chemosensing of plant-derived signals and -pheromone. Our study establishes V. dahliae as a suitable model for the analysis of fungal chemotropism and discovers new components of chemotropic signaling, during growth and host-pathogen interactions of V. dahliae.

microbiology↗

bioRxiv2021

Impairment of the cellulose degradation machinery enhances fungal virulence but limits reproductive fitness

Fungal endophytes grow in the apoplastic space, in constant contact with the plant cell wall (CW) that hinders microbe progression, while representing a source of nutrients. Although numerous fungal CW modifying proteins have been identified, their role during host colonization remains underexplored. Here we show that the root-infecting plant pathogen Fusarium oxysporum (Fo) does not require its complete arsenal of cellulases to infect the host plant. Quite the opposite, Fo mutants impaired in cellulose degradation become hypervirulent by enhancing the secretion of virulence factors. On the other hand, the reduction on cellulase activity had a severe negative effect on saprophytic growth and microconidia production during the final stages of the Fo infection cycle. These findings enhance our understanding on the function of plant CW degradation on the outcome of host-microbe interactions and reveal an unexpected role of cellulose degradation in a pathogens evolutionary success. TeaserUnexpectedly, fungi compromised in their capacity to degrade plant cellulose are hypervirulent but impaired in sporulation.

microbiology↗

bioRxiv2021

Conserved secreted effectors determine endophytic growth and multi-host plant compatibility in a vascular wilt fungus

Fungal interactions with plant roots, either beneficial or detrimental, have a major impact on agriculture and ecosystems. The soil inhabiting ascomycete Fusarium oxysporum (Fo) constitutes a species complex of worldwide distribution causing vascular wilt in more than a hundred different crops. Individual isolates of the fungus exhibit host-specific pathogenicity, determined by proteinaceous effectors termed secreted in xylem (SIX). However, such isolates can also colonize roots of non-host plants asymptomatically as endophytes, or even protect them against pathogenic isolates. The molecular determinants of multi-host plant colonization are currently unknown. Here, we identified a set of fungal effectors termed ERCs (Early Root Compatibility effectors), which are secreted during early biotrophic growth of Fo on both host and non-host plants. In contrast to the strain-specific SIX effectors, which are encoded on accessory genomic regions, ERCs are encoded on core regions and are found across the entire Fo species complex as well as in other phytopathogens, suggesting a conserved role in fungus-plant associations. Targeted deletion of ERC genes in a pathogenic Fo isolate resulted in reduced virulence on the host plant and rapid activation of plant immune responses, while in a non-pathogenic isolate it led to impaired root colonization and loss of biocontrol ability. Strikingly, some ERCs also contribute to Fo infection on the non-vascular land plant Marchantia polymorpha. Our results reveal an evolutionarily conserved mechanism for multi-host colonization by root infecting fungi.

plant biology↗

bioRxiv2021

Integration of chemosensing and carbon catabolite repression impacts fungal enzyme regulation and plant associations

Fungal metabolism and enzyme production are regulated by nutrient availability and by interactions with the living environment. We investigated the mechanisms underpinning adaptation of the biotechnological fungus Trichoderma reesei to decaying plant biomass versus living plants. We found that concentration-gated response to glucose, the main molecule sensed from dead plant biomass, is mediated by a conserved signaling pathway downstream of G protein-coupled receptors (GPCRs), while the carbon catabolite repressor CRE1 is critical for glucose concentration gating. The GPCRs CSG1 and CSG2 are further required for root colonization and formation of appressorium like structures on plant surfaces. Acceleration of sexual development in the presence of plant roots and their interactions with fruiting bodies indicates preferential association with plants. Our results reveal a complex sensing network governing resource distribution, enzyme production and fungal development that explains previously observed phenomena in fermentations and opens new perspectives for industrial strain improvement and agriculture.

microbiology↗

bioRxiv2021

Marchantia polymorpha model reveals conserved infection mechanisms in the vascular wilt fungal pathogen Fusarium oxysporum

The non-vascular plant Marchantia polymorpha has emerged as a valuable model for studying evolutionarily conserved microbial infection strategies and plant immune responses. However, only a handful of fungal pathogens of Marchantia have been described so far. Here we establish a new pathosystem using the root-infecting vascular wilt fungus Fusarium oxysporum. On angiosperms, this fungus exhibits exquisite adaptation to the plant vascular niche and host-specific pathogenicity, both of which are conferred by lineage-specific effectors secreted during growth in the xylem. We show that F. oxysporum isolates with different lifestyles - pathogenic or endophytic - are able to infect this non-vascular liverwort causing tissue maceration and plant cell killing. Similar to bacterial pathogens, F. oxysporum induces a PAMP-triggered immune response in M. polymorpha. Analysis of isogenic fungal mutants established that infection of Marchantia requires conserved fungal pathogenicity mechanisms such as mitogen activated protein kinases, transcriptional regulators and cell wall remodeling enzymes. Remarkably, lineage-specific virulence effectors are dispensable for infection, most likely due to the absence of xylem tissue in this non-vascular plant. The F. oxysporum - M. polymorpha system provides new insights into the mechanism and evolution of pathogenic and endophytic fungus-plant interactions. Significance statementRoot-infecting vascular fungi cause wilt diseases and provoke devastating losses in hundreds of crops. It is currently unknown how these pathogens evolved and whether they infect non-vascular plants, which diverged from vascular plants over 450 million years ago. Here we show that two strains of the fungus Fusarium oxysporum with opposed lifestyles, causing either wilting and death or beneficial protection on tomato, produce similar disease symptoms on the non-vascular plant Marchantia polymorpha. We define a set of core fungal pathogenicity factors required on both vascular and non-vascular plants and show that host-specific effectors contributing to disease on tomato are dispensable on Marchantia. These findings suggest that systemic wilt disease evolved in fungal pathogens after the emergence of vascular land plants.

plant biology↗

bioRxiv2020

A homologue of the mammalian tumour suppressor protein PTEN is a functional lipid phosphatase and required for chemotaxis in filamentous fungi

Phosphoinositides (PI) are essential components of eukaryotic membranes and function in a large number of signalling processes. While lipid second messengers are well studied in mammals and yeast, their role in filamentous fungi is poorly understood. We used fluorescent PI-binding molecular probes to localise the phosphorylated phosphatidylinositol species PI[3]P, PI[3,5]P2, PI[4]P and PI[4,5]P2 in hyphae of the endophyte Epichloe festucae in axenic culture and during interaction with its grass host Lolium perenne. We also analysed the roles of the phosphatidylinositol-4-phosphate 5-kinase MssD and the predicted phosphatidylinositol-3,4,5-triphosphate 3-phosphatase TepA, a homologue of the mammalian tumour suppressor protein PTEN. Deletion of tepA in E. festucae and in the root-infecting tomato pathogen Fusarium oxysporum had no impact on growth in culture or the host interaction phenotype. However, this mutation did uncover the presence of PI[3,4,5]P3 in septa of E. festucae and showed that TepA is required for chemotropism in F. oxysporum. The identification of PI[3,4,5]P3 in septa of{Delta} tepA strains suggests that filamentous fungi are able to generate PI[3,4,5]P3 using an alternative biosynthetic pathway and that fungal PTEN homologues are functional lipid phosphatases. The F. oxysporum chemotropism defect demonstrates a conserved role of PTEN homologues in chemotaxis across protists, fungi and mammals.

cell biology↗