Biology subjects

Wang, B.

Publications and source records attributed to Wang, B..

At least 613 records · Page 34Linked to original sources

bioRxiv2020

Bivalent binding of a fully human IgG to the SARS-CoV-2 spike proteins reveals mechanisms of potent neutralization

In vitro antibody selection against pathogens from naive combinatorial libraries can yield various classes of antigen-specific binders that are distinct from those evolved from natural infection1-4. Also, rapid neutralizing antibody discovery can be made possible by a strategy that selects for those interfering with pathogen and host interaction5. Here we report the discovery of antibodies that neutralize SARS-CoV-2, the virus responsible for the COVID-19 pandemic, from a highly diverse naive human Fab library. Lead antibody 5A6 blocks the receptor binding domain (RBD) of the viral spike from binding to the host receptor angiotensin converting enzyme 2 (ACE2), neutralizes SARS-CoV-2 infection of Vero E6 cells, and reduces viral replication in reconstituted human nasal and bronchial epithelium models. 5A6 has a high occupancy on the viral surface and exerts its neutralization activity via a bivalent binding mode to the tip of two neighbouring RBDs at the ACE2 interaction interface, one in the "up" and the other in the "down" position, explaining its superior neutralization capacity. Furthermore, 5A6 is insensitive to several spike mutations identified in clinical isolates, including the D614G mutant that has become dominant worldwide. Our results suggest that 5A6 could be an effective prophylactic and therapeutic treatment of COVID-19.

microbiology↗

bioRxiv2020

Cross-regulation between RpfG and HtsHs to regulate antibiotic biosynthesis in Lysobacter

Bacterial two-component systems (TCSs) sense and respond to environmental changes and modulate downstream gene expression. However, the mechanism of cross-talk between multiple TCSs is unclear. In this study, we report a previously uncharacterized mechanism by which the TCS protein RpfG interacts with hybrid two-component system (HyTCS) proteins HtsH1, HtsH2 and HtsH3 to regulate antibiotic biosynthesis in Lysobacter. RpfG, a phosphodiesterase (PDE), can degrade c-di-GMP to 5-pGpG and can regulate antibiotic heat-stable antifungal factor (HSAF) biosynthesis in a PDE- independent manner. Thus, we wondered whether RpfG regulate HSAF biosynthesis through interactions with other factors. Subsequently, we demonstrated that RpfG interacts with three HyTCS proteins (HtsH1, HtsH2 and HtsH3), that can inhibit the PDE enzymatic activity of RpfG. Importantly, deletion of htsH1, htsH2 and htsH3 resulted in significantly decreased HSAF production, and we showed that HtsH1, HtsH2 and HtsH3 depend on their phosphorylation activity to directly regulate HSAF biosynthesis gene expression. Our results reveal that RpfG does not depend on PDE activity to regulate HSAF biosynthesis, rather it interacts with HtsH1, HtsH2 and HtsH3 to do so, a regulatory mechanism that may be a conserved paradigm in Lysobacter and Xanthomonas.

microbiology↗

bioRxiv2020

Single-cell analysis of Schistosoma mansoni reveals a conserved genetic program controlling germline stem cell fate

Schistosomes are parasitic flatworms causing one of the most prevalent infectious diseases from which millions of people are currently suffering. Their germline outputs many fertilized eggs, which are both the transmissible agents and the cause of the infection-associated pathology. Given its significance, the schistosome germline has been a research focus for more than a century. Nonetheless, little is known about the molecular mechanisms that regulate its development. Here, we construct a transcriptomic cell type atlas of juvenile schistosomes. This allows us to capture germline stem cells (GSCs) during de novo gonadal development. We identify a genetic program that balances the fate of GSC between proliferation and differentiation. This program is controlled by onecut, a homeobox transcription factor, and boule, an mRNA binding protein. Evaluating this genetic program in schistosomes free-living evolutionary cousin, the planarian, shows that this germline-specific regulatory program is conserved but its function has changed significantly during evolution.

developmental biology↗

bioRxiv2020

Deviation from baseline mutation burden provides powerful and robust rare-variants association test for complex diseases

The identification of rare variants that contribute to complex diseases is challenging due to low statistical power. Here we propose a novel and powerful rare variants association test based on the deviation of the observed mutational burden in a genomic region from a baseline mutation burden predicted by weighted recursive truncated negative-binomial regression (RUNNER) on genomic features available from public data. Simulation studies show that RUNNER is substantially more powerful than state-of-the-art rare variant association methods (including SKAT, CMC and KBAC), while maintaining correct type 1 error rates under population stratification and in small samples. Applied to real data, RUNNER “rediscovered” known genes of Hirschsprung disease missed by current methods, and detected promising new candidate genes, including NXPE4 for Hirschsprung disease and CXCL16 for Alzheimer’s disease. The proposed approach provides a powerful and robust method to identify rare risk variants for complex diseases.Competing Interest StatementThe authors have declared no competing interest.View Full Text

genetics↗

bioRxiv2020

Unravel the Mystery of NIC1-locus on Nicotine Biosynthesis Regulation in Tobacco

ABSTRACTBackground Nicotine biosynthesis is mainly regulated by jasmonate (JA) signaling cascade in Nicotiana tabacum. As an allotetraploid species, the regulation of nicotine biosynthesis has been genetically verified via two unlinked NIC loci (named as NIC1 and NIC2) which are possibly originated from its two ancestral diploids. Previously, a N. tomentosiformis originated ethylene response factor (ERF) gene cluster was identified as the NIC2-locus which has been demonstrated positively regulates nicotine accumulation in N. tabacum.Results Here, we describe the genetic mapping of NIC1-locus, the major nicotine regulatory locus, by using a NIC1-locus segregating population through bulked segregant analysis. We identified two linkage marker TM23004 and TM22038 were delimited the NIC1-locus within a ~34.3-Mb genomic region at pseudochromosome 07 of tobacco genome. Genomic scan within this region revealed a NIC2-like locus ERF gene cluster exist in. To verify this ERF gene cluster is the genetically called “NIC1-locus”, different functional experiments based on most of the ERFs in regulating nicotine biosynthesis and their influences on alkaloid accumulations have been carried out. Collinearity analysis showed that NIC1-locus ERF genes are originated from N. sylvestris and exclusively expressed in root tissues. In addition, transcriptomic results indicate that NIC1-locus ERF genes are coexpressed with the NIC2-locus ERF genes and other nicotine biosynthetic genes and regulators after JA induction. Furthermore, the suppressed expression of four ERFs of the NIC1-locus genes corresponding with decreased NtPMT and NtQPT expression in NtMYC2-RNAi lines indicates the selected NIC1-locus ERFs function in downstream of NtMYC2 in the JA signaling cascades. In the meanwhile, the alkaloid levels are also determined by the amplitude of the four ERF gene expressions in both wild type and LA mutant. Additionally, in vitro binding assays, transient activation assays, and ectopic expression in transgenic plants demonstrate that these ERF genes are able to bind the GCC-box elements residing in the step-limiting gene promoters (such as NtPMT2, NtQPT2) and functional redundant but quantitatively transactivate nicotine biosynthetic gene expression. For nic1-locus mutation, two different sizes of deletions (nic1-S and nic1-B) were identified which occurred at the surrounding regions of the NIC1-locus gene cluster, which might disrupt, to some extent, chromosomal microenvironment and change gene expression around the deletion regions (including NIC1-locus ERFs), resulting in the decreased expression levels of NIC1-locus ERFs (such as NtERF199) and reduced alkaloid accumulation in the nic1-locus mutant.Conclusions Our findings not only provide insight in to the mechanism of the NIC1-locus ERFs in the regulatory network of nicotine biosynthesis, but also unraveled the theoretical basis of the nic1-locus mutation in low nicotine mutant. These functional verified NIC1-locus ERF genes can be further used as potential target(s) for ethyl methanesulfonate-based mutagenesis to manipulate nicotine level in tobacco variety in tobacco breeding program.Competing Interest StatementThe authors have declared no competing interest.AbbreviationsA622a PIP family oxidoredutase for nicotine precursors condensationODCornithine decarboxylaseADCarginine decarboxylasePMTputrescine N-methyltransferaseMPON-methylputrescine oxidaseAOaspartate oxidaseQSquinolinic acid synthaseQPTqunolinic acid phosphoribosyl transferaseSPDSspermidine synthaseSAMSS-adenosylmethionine synthaseSAMDCS-adenosylmethione decarboxylasePCRPolymerase chain reactionRNA-seqRNA SequencingRPKMReads Per Kilobase per Million mapped readsSSRsimple sequence repeatqRT-PCRQuantitative real-time PCRCRchromosome rearrangementCNVcopy number variantView Full Text

plant biology↗

bioRxiv2020

Upgraded CRISPR/Cas9 Tools for Tissue-Specific Mutagenesis in Drosophila

ABSTRACTCRISPR/Cas9 has emerged as a powerful technology for tissue-specific mutagenesis. However, tissue-specific CRISPR/Cas9 tools currently available in Drosophila remain deficient in three significant ways. First, many existing gRNAs are inefficient, such that further improvements of gRNA expression constructs are needed for more efficient and predictable mutagenesis in both somatic and germline tissues. Second, it has been difficult to label mutant cells in target tissues with current methods. Lastly, application of tissue-specific mutagenesis at present often relies on Gal4-driven Cas9, which hampers the flexibility and effectiveness of the system. Here we tackle these deficiencies by building upon our previous CRISPR-mediated tissue restricted mutagenesis (CRISPR-TRiM) tools. First, we significantly improved gRNA efficiency in somatic tissues by optimizing multiplexed gRNA design. Similarly, we also designed efficient dual-gRNA vectors for the germline. Second, we developed methods to positively and negatively label mutant cells in tissue-specific mutagenesis by incorporating co-CRISPR reporters into gRNA expression vectors. Lastly, we generated genetic reagents for convenient conversion of existing Gal4 drivers into tissue-specific Cas9 lines based on homology-assisted CRISPR knock-in (HACK). In this way, we expand the choices of Cas9 for CRISPR-TRiM analysis to broader tissues and developmental stages. Overall, our upgraded CRISPR/Cas9 tools make tissue-specific mutagenesis more versatile, reliable, and effective in Drosophila. These improvements may be also applied to other model systems.Competing Interest StatementThe authors have declared no competing interest.View Full Text

genetics↗

bioRxiv2020

Gazing into the Metaboverse: Automated exploration and contextualization of metabolic data

Metabolism forms a complex, interdependent network, and perturbations can have indirect effects that are pervasive. Identifying these patterns and their consequences is difficult, particularly when the effects occur across canonical pathways, and these difficulties have long acted as a bottleneck in metabolic data analysis. This challenge is compounded by technical limitations in metabolomics approaches that garner incomplete datasets. Current network-based tools generally utilize pathway-level analysis lacking the granular resolution required to provide context into the effects of all perturbations, regardless of magnitude, across the metabolic network. To address these shortcomings, we introduce algorithms that allow for the real-time extraction of regulatory patterns and trends from user data. To minimize the impact of missing measurements within the metabolic network, we introduce methods that enable complex pattern recognition across multiple reactions. These tools are available interactively within the user-friendly Metaboverse app (https://github.com/Metaboverse) to facilitate exploration and hypothesis generation. We demonstrate that expected signatures are accurately captured by Metaboverse. Using public lung adenocarcinoma data, we identify a previously undescribed multi-dimensional signature that correlated with survival outcomes in lung adenocarcinoma patients. Using a model of respiratory deficiency, we identify relevant and previously unreported regulatory patterns that suggest an important compensatory role for citrate during mitochondrial dysfunction. This body of work thus demonstrates that Metaboverse can identify and decipher complex signals from data that have been otherwise difficult to identify with previous approaches.

biochemistry↗

bioRxiv2020

MAGIC: Mosaic Analysis by gRNA-Induced Crossing-over

Mosaic animals have provided the platform for many fundamental discoveries in developmental biology, cell biology, and other fields. Techniques to produce mosaic animals by mitotic recombination have been extensively developed in Drosophila melanogaster but are less common for other laboratory organisms. Here, we report mosaic analysis by gRNA-induced crossing-over (MAGIC), a new technique for generating mosaic animals based on DNA double-strand breaks produced by CRISPR/Cas9. MAGIC efficiently produces mosaic clones in both somatic tissues and the germline of Drosophila. Further, by developing a MAGIC toolkit for one chromosome arm, we demonstrate the method’s application in characterizing gene function in neural development and in generating fluorescently marked clones in wild-derived Drosophila strains. Eliminating the need to introduce recombinase-recognition sites in the genome, this simple and versatile system simplifies mosaic analysis in Drosophila and can be applied in any organism that is compatible with CRISPR/Cas9.Competing Interest StatementThe authors have declared no competing interest.View Full Text

genetics↗

bioRxiv2020

Phagocytosis drives NAD+ reduction-induced dendrite degeneration in Drosophila

After injury, severed dendrites and axons expose the "eat-me" signal phosphatidylserine (PS) on their surface and degenerate by disassembly. While axon degeneration is controlled by a conserved "axon-death" pathway that is thought to activate self-destruction, how PS exposure is regulated by this pathway and whether PS-induced phagocytosis contributes to neurite breakdown in vivo remain unknown. Here we show that in Drosophila sensory dendrites, PS exposure and self-destruction are triggered by two distinct levels of NAD+ reduction downstream of Sarm activation. Surprisingly, phagocytosis is the main driver of dendrite degeneration induced by both genetic NAD+ disruptions and injury. Furthermore, the axon-death factor Axed is only partially required for self-destruction of injured dendrites, acting in parallel with PS-induced phagocytosis. Lastly, injured dendrites exhibit a unique rhythmic calcium flashing that correlates with self-destruction. Therefore, a special genetic program coordinates PS exposure and self-destruction in injury-induced dendrite degeneration in vivo.

cell biology↗

bioRxiv2020

Proto-sex locus in large yellow croaker provides insights into early evolution of the sex chromosome

Autosomal origins of heterogametic sex chromosomes have been inferred frequently from suppressed recombination and gene degeneration manifested in incompletely differentiated sex chromosomes. However, the initial transition of an autosome region to a proto-sex locus has been not explored in depth. By assembling and analyzing a chromosome-level draft genome, we found a recent (evolved 0.26 million years ago), highly homologous, and dmrt1 containing sex-determination locus with slightly reduced recombination in large yellow croaker (Larimichthys crocea), a teleost species with genetic sex determination (GSD) and with undifferentiated sex chromosomes. We observed genomic homology and polymorphic segregation of the proto-sex locus between sexes. Expression of dmrt1 showed a stepwise increase in the development of testis, but not in the ovary. We infer that the inception of the proto-sex locus involves a few divergences in nucleotide sequences and slight suppression of recombination in an autosome region. In androgen-induced sex reversal of genetic females, in addition to dmrt1, genes in the conserved dmrt1 cluster, and the rest of the sex determination network were activated. We provided evidence that broad functional links were shared by genetic sex determination and environmental sex reversal.

evolutionary biology↗

bioRxiv2020

Early temporal dynamics of cellular responses to SARS-CoV-2

Type I interferons (IFNs) are our first line of defence against a virus. Protein over-expression studies have suggested the ability of SARS-CoV-2 proteins to block IFN responses. Emerging data also suggest that timing and extent of IFN production is associated with manifestation of COVID-19 severity. In spite of progress in understanding how SARS-CoV-2 activates antiviral responses, mechanistic studies into wildtype SARS-CoV-2-mediated induction and inhibition of human type I IFN responses are lacking. Here we demonstrate that SARS-CoV-2 infection induces a mild type I IFN response in vitro and in moderate cases of COVID-19. In vitro stimulation of type I IFN expression and signaling in human airway epithelial cells is associated with activation of canonical transcriptions factors, and SARS-CoV-2 is unable to inhibit exogenous induction of these responses. Our data demonstrate that SARS-CoV-2 is not adept in blocking type I IFN responses and provide support for ongoing IFN clinical trials. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/158154v2_ufig1.gif" ALT="Figure 1"> View larger version (35K): org.highwire.dtl.DTLVardef@193c540org.highwire.dtl.DTLVardef@7b106forg.highwire.dtl.DTLVardef@1741cfforg.highwire.dtl.DTLVardef@1bde68_HPS_FORMAT_FIGEXP M_FIG GRAPHICAL SUMMARY C_FIG

immunology↗

bioRxiv2020

Double Emulsion Picoreactors for High-Throughput Single-Cell Encapsulation and Phenotyping via FACS

In the past five years, droplet microfluidic techniques have unlocked new opportunities for the high-throughput genome-wide analysis of single cells, transforming our understanding of cellular diversity and function. However, the field lacks an accessible method to screen and sort droplets based on cellular phenotype upstream of genetic analysis, particularly for large and complex cells. To meet this need, we developed Dropception, a robust, easy-to-use workflow for precise single-cell encapsulation into picoliter-scale double emulsion droplets compatible with high-throughput phenotyping via fluorescence-activated cell sorting (FACS). We demonstrate the capabilities of this method by encapsulating five standardized mammalian cell lines of varying size and morphology as well as a heterogeneous cell mixture of a whole dissociated flatworm (5 - 25 m in diameter) within highly monodisperse double emulsions (35 m in diameter). We optimize for preferential encapsulation of single cells with extremely low multiple-cell loading events (<2% of cell-containing droplets), thereby allowing direct linkage of cellular phenotype to genotype. Across all cell lines, cell loading efficiency approaches the theoretical limit with no observable bias by cell size. FACS measurements reveal the ability to discriminate empty droplets from those containing cells with good agreement to single-cell occupancies quantified via microscopy, establishing robust droplet screening at single-cell resolution. High-throughput FACS phenotyping of cellular picoreactors has the potential to shift the landscape of single-cell droplet microfluidics by expanding the repertoire of current nucleic acid droplet assays to include functional screening. ABSTRACT FIGURE O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=85 SRC="FIGDIR/small/139311v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@9d2028org.highwire.dtl.DTLVardef@1aa55b3org.highwire.dtl.DTLVardef@1e05eb3org.highwire.dtl.DTLVardef@1695a88_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

bioRxiv2020

VirusDIP: Virus Data Integration Platform

MotivationThe Coronavirus Disease 2019 (COVID-19) pandemic poses a huge threat to human public health. Viral sequence data plays an important role in the scientific prevention and control of epidemics. A comprehensive virus database will be vital useful for virus data retrieval and deep analysis. To promote sharing of virus data, several virus databases and related analyzing tools have been created. ResultsTo facilitate virus research and promote the global sharing of virus data, we present here VirusDIP, a one-stop service platform for archive, integration, access, analysis of virus data. It accepts the submission of viral sequence data from all over the world and currently integrates data resources from the National GeneBank Database (CNGBdb), Global initiative on sharing all influenza data (GISAID), and National Center for Biotechnology Information (NCBI). Moreover, based on the comprehensive data resources, BLAST sequence alignment tool and multi-party security computing tools are deployed for multi-sequence alignment, phylogenetic tree building and global trusted sharing. VirusDIP is gradually establishing cooperation with more databases, and paving the way for the analysis of virus origin and evolution. All public data in VirusDIP are freely available for all researchers worldwide. Availabilityhttps://db.cngb.org/virus/ Contactweixiaofeng@cngb.org

bioinformatics↗

bioRxiv2020

C3: Connect separate Connected Components to form a succinct disease module

Accurate disease module is helpful in understanding the molecular mechanism of disease causation and identifying drug target. However, for the fragmentization of disease module in incomplete human interactome, how to determine connectivity pattern and detect a full neighbourhood of disease is an open problem. In this paper, a topology-based method is developed to dissect the connectivity of intermediate nodes and edges and form a succinct disease module. By applying this Connect separate Connected Components (CCC, C3) method on a large corpus of curated diseases, we find that most Separate Connected Components (SCCs) formed by Disease-Associated Proteins (DAPs) can be connected into a well-connected component as a succinct observable module. This pattern also holds for altered genes from multi-omics data such as The Cancer Genome Atlas. Overall, C3 tool can not only inspire a deeper understanding of interconnectedness of phenotypically related genes and different omics data, but also be used to detect a well-defined neighbourhood that drives complex pathological processes.

bioinformatics↗

bioRxiv2020

Iron Supplementation Eliminates Antagonistic Interactions Between Root Associated Bacteria

The rhizosphere microbiome (rhizobiome) plays a critical role in plant health and development. However the processes by which the constituent microbes interact to form and maintain a community are not well understood. To investigate these molecular processes, we examined pairwise interactions between 11 different microbial isolates under selected nutrient-rich and nutrient-limited conditions. We observed that when grown with media supplemented with 56 mM glucose, 2 microbial isolates were able to inhibit the growth of 6 out of 11 other microbes tested. The interaction between microbes persisted even after the antagonistic microbe was removed, upon exposure to spent media. To probe the genetic basis for these antagonistic interactions, we used a barcoded transposon library in a proxy bacterium, Pseudomonas putida, to identify genes which showed enhanced sensitivity to the antagonistic factor(s) secreted by Acinetobacter sp. 02. Iron metabolism-related gene clusters in P. putida were implicated by this systems-level analysis. The supplementation of iron prevented the antagonistic interaction in the original microbial pair supporting the hypothesis that iron limitation drives antagonistic microbial interactions between rhizobionts. We conclude that rhizobiome community composition is influenced by competition for limiting nutrients with implications for growth and development of the plant.

microbiology↗

bioRxiv2020

CDK4/6 inhibition promotes senescent states with restricted secretory phenotype and reduced toxicity

Cellular senescence is a state of stable growth arrest that acts as a tumor suppressive mechanism. Several anti-cancer interventions function partly by inducing malignant cells into senescence. However, because of systemic administration and lack of specificity, anti-cancer treatments are associated with premature senescence of various non-malignant cells. Therapy-induced non-malignant senescent cells can have profound detrimental pro-tumorigenic and pro-disease functions via activation of a pro-inflammatory and NF-{kappa}B-mediated secretory phenotype (SASP). Inhibitors of the cyclin-dependent kinases 4/6 (CDK4/6i) has recently shown to have potent cytostatic effects with reduced toxicities. Here, we show that CDK4/6i lead non-malignant cells to a senescent state that lacks the pro-inflammatory and NF-{kappa}B-associated SASP. Interestingly, CDK4/6i-induced senescence overexpressed a number of genes encoding for secreted proteins, which we show being dependent on p53 transcriptional activity. CDK4/6i-induced p16+ senescent cells with a p53-associated (PASP), but not NF-{kappa}B-associated (NASP), secretory phenotype do not exert detrimental and pro-tumorigenic functions, but still retain the capacity to induce paracrine senescence and undergo clearance in vivo. Our data suggest that that senescent cells with a PASP but without a NASP may be well-tolerated and may represent a less toxic outcome for cancer interventions.

cell biology↗

bioRxiv2020

Pituitary stem cells produce paracrine WNT signals to control the expansion of their descendant progenitor cells

In response to physiological demand, the pituitary gland generates new hormone-secreting cells from committed progenitor cells throughout life. It remains unclear to what extent pituitary stem cells (PSCs), which uniquely express SOX2, contribute to pituitary growth and renewal. Moreover, neither the signals that drive proliferation nor their sources have been elucidated. We have used genetic approaches in the mouse, showing that the WNT pathway is essential for proliferation of all lineages in the gland. We reveal that SOX2+ stem cells are a key source of WNT ligands. By blocking secretion of WNTs from SOX2+ PSCs in vivo, we demonstrate that proliferation of neighbouring committed progenitor cells declines, demonstrating that progenitor multiplication depends on the paracrine WNT secretion from SOX2+ PSCs. Our results indicate that stem cells can hold additional roles in tissue expansion and homeostasis, acting as paracrine signalling centres to coordinate the proliferation of neighbouring cells.

developmental biology↗

bioRxiv2020

Chromosome-scale genome assembly of Fusarium oxysporum strain Fo47, a fungal endophyte and biocontrol agent

Here, we report a chromosome-level genome assembly of Fusarium oxysporum strain Fo47 (12 pseudomolecules; contig N50: 4.52Mb), generated using a combination of PacBio long-read, Illumina pair-ended and Hi-C sequencing data. Although F. oxysporum causes vascular wilt to over 100 plant species, the strain Fo47 is classified as an endophyte and widely used as a biocontrol agent for plant disease control. The Fo47 genome carries a single accessory chromosome of 4.23 Mb, compared to the reference genome of F. oxysporum f.sp. lycopersici strain Fol4287. The high-quality assembly and annotation of the Fo47 genome will be a valuable resource for studying the mechanisms underlying the endophytic interactions between F. oxysporum and plants, as well as deciphering the genome evolution of the F. oxysporum species complex.

genomics↗