The objective of this symposium is to create a scientific event that is at the forefront of fundamental research in beneficial plant-microbe interactions.
The symposium will bring together about 150 participants in a rather informal atmosphere, facilitating exchanges. We also aim at proposing a highly attractive program at a moderate inscription fee to give the opportunity to researchers - in particular those at the early stage of their career – to participate to an exciting top-level scientific event. Young researchers will have the opportunity to present their work with a poster.
Efficient strategies for limiting the impact of pathogens on crops require a good understanding of the factors underlying the evolution of compatibility range for the pathogens and host plants, i.e., the set of host genotypes that a particular pathogen genotype can infect and the set of pathogen genotypes that can infect a particular host genotype. Until now, little is known about the evolutionary and ecological factors driving compatibility ranges in systems implicating crop plants. We studied the evolution of host and pathogen compatibility ranges for rice blast disease, which is caused by the ascomycete Magnaporthe oryzae. We challenged 61 rice varieties from three rice subspecies with 31 strains of M. oryzae collected worldwide from all major known genetic groups. We determined the compatibility range of each plant variety and pathogen genotype and the severity of each plant−pathogen interaction. Compatibility ranges differed between rice subspecies, with the most resistant subspecies selecting for pathogens with broader compatibility ranges and the least resistant subspecies selecting for pathogens with narrower compatibility ranges. These results are consistent with a nested distribution of R genes between rice subspecies.
Background: To cause an economically important blast disease on rice, the filamentous fungus Magnaporthe oryzae forms a specialized infection structure, called an appressorium, to penetrate host cells. Once inside host cells, the fungus produces a filamentous primary hypha that differentiates into multicellular bulbous invasive hyphae (IH), which are surrounded by a host-derived membrane. These hyphae secrete cytoplasmic effectors that enter host cells presumably via the biotrophic interfacial complex (BIC). The first IH cell, also known as the side BIC-associated cell, is a specialized effector-secreting cell essential for a successful infection. This study aims to determine cellular processes that lead to the development of this effector-secreting first IH cell inside susceptible rice cells. Results: Using live-cell confocal imaging, we determined a series of cellular events by which the appressorium gives rise to the first IH cell in live rice cells. The filamentous primary hypha extended from the appressorium and underwent asymmetric swelling at its apex. The single nucleus in the appressorium divided, and then one nucleus migrated into the swollen apex. Septation occurred in the filamentous region of the primary hypha, establishing the first IH cell. The tip BIC that was initially associated with the primary hypha becomes the side BIC on the swollen apex prior to nuclear division in the appressorium. The average distance between the early side BIC and the nearest nucleus in the appressorium was estimated to be more than 32 μm. These results suggest an unknown mechanism by which effectors that are expressed in the appressorium are transported through the primary hypha for their secretion to the distantly located BIC. When M. oryzae was inoculated on heat-killed rice cells, penetration proceeded as normal, but there was no differentiation of a bulbous IH cell, suggesting its specialization for establishment of biotrophic infection. Conclusions: Our studies reveal cellular dynamics associated with the development of the effector-secreting first IH cell. Our data raise new mechanistic questions concerning hyphal differentiation in response to host environmental cues and effector trafficking from the appressorium to the BIC.
Successful colonization of plants by prokaryotic and eukaryotic pathogens requires active effector-mediated suppression of defense responses and host tissue reprogramming. Secreted effector proteins can either display their activity in the apoplast or translocate into host cells and function therein. Although characterized in bacteria, the molecular mechanisms of effector delivery by fungal phytopathogens remain elusive.
Here we report the establishment of an assay that is based on biotinylation of effectors in the host cytoplasm as hallmark of uptake. The assay exploits the ability of the bacterial biotin ligase BirA to biotinylate any protein that carries a short peptide (Avitag). It is based on the stable expression of BirA in the cytoplasm of maize plants and on engineering of Ustilago maydis strains to secrete Avitagged effectors.
We demonstrate translocation of a number of effectors in the U. maydis–maize system and show data that suggest that the uptake mechanism could be rather nonspecific
The assay promises to be a powerful tool for the classification of effectors as well as for the functional study of effector uptake mechanism not only in the chosen system but more generally for systems where biotrophic interactions are established.
Plants detect conserved molecular patterns of pathogens via cell surface-localized receptors, such as the flagellin receptor kinase FLS2, that initiate effective plant immunity. Activated FLS2 is endocytosed, but the degree to which other receptor kinases exhibit similar spatiotemporal dynamics remains unclear. We show that internalization into a common endosomal pathway after ligand perception is a general phenomenon of the tested receptor kinases, including the danger peptide receptor PEPR1. FLS2 endocytosis is mediated by clathrin and is uncoupled from the regulation of acute pathogen-induced responses, but is involved in steady defenses and contributes to plant immunity against bacterial infection. We propose that clathrin-dependent internalization of ligand-activated receptor kinases into a common endosomal pathway facilitates the responses required for full plant immunity.
In the 21st century, the wheat stripe rust fungus has evolved to be the largest biotic limitation to global wheat production. New pathogen genotypes are more aggressive and able to infect previously resistant wheat varieties, leading to rapid pathogen migration across and between continents. We now know the full life cycle, microevolutionary relationships and past migration routes on a global scale. Current sequencing technologies have provided the first fungal draft genomes and simplified plant resistance gene cloning. Yet, we know nothing about the molecular and microevolutionary mechanisms that facilitate the infection process and cause new devastating pathogen races. These are the questions that need to be addressed by exploiting the synergies between novel 21st century biology tools and decades of dedicated pathology work.
Plants and animals detect the presence of potential pathogens through the perception of conserved microbial patterns by cell surface receptors. Certain solanaceous plants, including tomato, potato and pepper, detect flgII-28, a region of bacterial flagellin that is distinct from that perceived by the well-characterized FLAGELLIN-SENSING 2 receptor. Here we identify and characterize the receptor responsible for this recognition in tomato, called FLAGELLIN-SENSING 3. This receptor binds flgII-28 and enhances immune responses leading to a reduction in bacterial colonization of leaf tissues. Further characterization of FLS3 and its signalling pathway could provide new insights into the plant immune system and transfer of the receptor to other crop plants offers the potential of enhancing resistance to bacterial pathogens that have evolved to evade FLS2-mediated immunity.
This special issue is dedicated to these topics, featuring research articles as well as review papers. Early communication, from chemotaxis, recognition of the microbes by the plant, effective colonization, and the plant genes necessary for positive response to the microorganisms are the focus of nine of the papers. Biotic stress tolerance conferred by plant-associated microorganisms against insects and microbial pathogens is covered in three papers. Increased tolerance to abiotic factors including salinity and limited nutrients as well as overall increased growth and health are the topics of three of the papers. Many of the authors included future perspectives on how to move this important research field forward. Information gained from plant–microbe interaction studies in native habitats may be especially relevant since the host plant and microorganisms have co-evolved with opportunities by the plant to select over time the most beneficial symbionts. Understanding the requirements for recruitment, recognition, colonization, and response will be essential if this knowledge is to be applied to commercial agriculture. Determination of the mechanisms by which microbiota impart tolerance to biotic and abiotic stress will enable optimization for improved plant health and growth under the increased challenges resulting from climate change.
Elicitins are structurally conserved extracellular proteins in Phytophthora and Pythium oomycete pathogen species. They were first described in the late 1980s as abundant proteins in Phytophthora culture filtrates that have the capacity to elicit hypersensitive (HR) cell death and disease resistance in tobacco. Later, they became well-established as having features of microbe-associated molecular patterns (MAMPs) and to elicit defences in a variety of plant species. Research on elicitins culminated in the recent cloning of the elicitin response (ELR) cell surface receptor-like protein, from the wild potato Solanum microdontum, which mediates response to a broad range of elicitins. In this review, we provide an overview on elicitins and the plant responses they elicit. We summarize the state of the art by describing what we consider to be the nine most important features of elicitin biology.
Herbivore selection of plant hosts and plant responses to insect colonization have been subjects of intense investigations. A growing body of evidence suggests that for successful colonization to occur, (effector/virulence) proteins in insect saliva must modulate plant defense responses to the benefit of the insect. A range of insect saliva proteins that modulate plant defense responses have been identified, but there is no direct evidence that these proteins are delivered into specific plant tissues and enter plant cells. Aphids and other sap-sucking insects of the order Hemiptera use their specialized mouthparts (stylets) to probe plant mesophyll cells, until they reach the phloem cells for long-term feeding. Here we show by immunogold-labeling of ultrathin sections of aphid feeding sites that an immuno-suppressive aphid effector localizes in the cytoplasm of mesophyll cells near aphid stylets, but not in cells further away from aphid feeding sites. In contrast, another aphid effector protein localizes in the sheaths composed of gelling saliva that surround the aphid stylets. Thus, insects deliver effectors directly into plant tissue. Moreover, different aphid effectors locate extracellularly in the sheath saliva or are introduced into the cytoplasm of plant cells.
INVERNESS, Calif. — At the height of California’s fierce wildfire season, the Sierra Nevada and North Coast forests are choked with tens of millions of dead and dying trees, from gnarly oaks to elegant pines that are turning leafy chapels into tinderboxes of highly combustible debris.
Ground crews wielding chain saws, axes and wood chippers are braving the intense summer heat in the Sierra’s lower elevations, where most of the pine trees have died. The devastation and danger are greatest in the central and southern Sierra Nevada, where the estimated number of dead trees since 2010 is a staggering 66 million.
Scientists say rarely is one culprit to blame for the escalation in the state’s tree deaths, and the resulting fire hazard. Rather, destruction on such a broad scale is nearly always the result of a complex convergence of threats to forest ecosystems.
Chief among them is a severe, sustained drought in the Sierra Nevada that is stressing trees and disabling their natural defenses. Climate change is raising temperatures, making for warmer winters. No longer kept in check by winter’s freeze, bark beetle populations are growing. Separately, a nonnative, potent plant pathogen is thriving in the moist areas of the North Coast, introduced to California soil by global trade. Opportunistic fungi are standing by, ready to finish the kill.
Factor in human shortcomings — poor or absent forest management, a failure to clear out ignitable dead wood, the darker temptation of arson, unchecked carelessness — and you have a lethal recipe.
“It’s never just one thing that brings down trees,” said David Rizzo, the chairman of plant pathology at the University of California, Davis. “It’s always a combination. The first may weaken trees; the next stresses trees over time. Then comes a third, shutting down the trees’ immune and defense systems. Finally, the last may come along to disrupt nutrient systems. When all this happens at once, or in rapid succession, trees are no longer able to save themselves.”
Two of California’s prized forest regions are in failing health because such conditions have stacked the odds against them. In the Sierra Nevada, the losses of pines and other conifers are concentrated and widening.
Along the North Coast, a picturesque blink of a town called Inverness and the surrounding Marin County woodlands are “ground zero,” Dr. Rizzo said, for the mysterious plant pathogen that began infesting coast oaks probably as far back as the mid-1980s.
Dr. Rizzo, who closely studies Phytophthora ramorum, also known as sudden oak death, returns often to this cozy glen on a peninsula overlooking the clear blue water. Graduate students, research associates and others accompany him to this patch of forest serving as an outdoor classroom, laboratory and demonstration plot.
It took years of research — detective work, really — before experts like Dr. Rizzo and Matteo Garbelotto, a professor of environmental science policy and management at the University of California, Berkeley, discerned that the funguslike pathogen had infested coast oaks years before their showy demise.
Dr. Rizzo estimated that five million to 10 million coastal trees had died because of sudden oak death.
A related pathogen, Phytophthora infestans, was responsible for the Great Potato Famine in Ireland in the mid-1800s.
Background. Rust fungi are an important group of plant pathogens that cause devastating losses in agricultural, silvicultural and natural ecosystems. Plants can be protected from rust disease by resistance genes encoding receptors that trigger a highly effective defence response upon recognition of specific pathogen avirulence proteins. Identifying avirulence genes is crucial for understanding how virulence evolves in the field.
Results. To facilitate avirulence gene cloning in the flax rust fungus, Melampsora lini, we constructed a high-density genetic linkage map using single nucleotide polymorphisms detected in restriction site-associated DNA sequencing (RADseq) data. The map comprises 13,412 RADseq markers in 27 linkage groups that together span 5860 cM and contain 2756 recombination bins. The marker sequences were used to anchor 68.9 % of the M. lini genome assembly onto the genetic map. The map and anchored assembly were then used to: 1) show that M. lini has a high overall meiotic recombination rate, but recombination distribution is uneven and large coldspots exist; 2) show that substantial genome rearrangements have occurred in spontaneous loss-of-avirulence mutants; and 3) identify the AvrL2 and AvrM14 avirulence genes by map-based cloning. AvrM14 is a dual-specificity avirulence gene that encodes a predicted nudix hydrolase. AvrL2 is located in the region of the M. lini genome with the lowest recombination rate and encodes a small, highly-charged proline-rich protein.
Conclusions. The M. lini high-density linkage map has greatly advanced our understanding of virulence mechanisms in this pathogen by providing novel insights into genome variability and enabling identification of two new avirulence genes.
Filamentous plant pathogens deliver effector proteins to host cells to promote infection. The Phytophthora infestans RXLR-type effector PexRD54 binds potato ATG8 via its ATG8-family interacting motif (AIM) and perturbs host selective autophagy. However, the structural basis of this interaction remains unknown. Here we define the crystal structure of PexRD54, which comprises a modular architecture including five tandem repeat domains, with the AIM sequence presented at the disordered C-terminus. To determine the interface between PexRD54 and ATG8, we solved the crystal structure of potato ATG8CL in complex with a peptide comprising the effectors AIM sequence, and established a model of the full-length PexRD54/ATG8CL complex using small angle X-ray scattering. Structure-informed deletion of the PexRD54 tandem domains reveals retention of ATG8CL binding in vitro and in planta. This study offers new insights into structure/function relationships of oomycete RXLR effectors and how these proteins engage with host cell targets to promote disease.
• The Phytophthora haustorium is a major site of secretion during infection.
• The host endocytic cycle contributes to biogenesis of the Extra-Haustorial Membrane. • RXLR effectors manipulate host processes at diverse subcellular locations.
• They directly manipulate the activity or location of immune proteins.
• They also promote the activity of endogenous negative regulators of immunity.
Late blight, caused by the oomycete Phytophthora infestans, is a major global disease of potato and tomato. Cell biology is teaching us much about the developmental stages associated with infection, especially the haustorium, which is a site of intimate interaction and molecular exchange between pathogen and host. Recent observations suggest a role for the plant endocytic cycle in specific recruitment of host proteins to the Extra-Haustorial Membrane, emphasising the unique nature of this membrane compartment. In addition, there has been a strong focus on the activities of RXLR effectors, which are delivered into plant cells to modulate and manipulate host processes. RXLR effectors interact directly with diverse plant proteins at a range of subcellular locations to promote disease.
Magnaporthe oryzae, the fungus causing rice blast disease, should contend with host innate immunity to develop invasive hyphae (IH) within living host cells. However, molecular strategies to establish the biotrophic interactions are largely unknown. Here, we report the biological function of a M. oryzae-specific gene, Required-for-Focal-BIC-Formation 1 (RBF1). RBF1expression was induced in appressoria and IH only when the fungus was inoculated to living plant tissues. Long-term successive imaging of live cell fluorescence revealed that the expression of RBF1 was upregulated each time the fungus crossed a host cell wall. Like other symplastic effector proteins of the rice blast fungus, Rbf1 accumulated in the biotrophic interfacial complex (BIC) and was translocated into the rice cytoplasm. RBF1-knockout mutants (Δrbf1) were severely deficient in their virulence to rice leaves, but were capable of proliferating in abscisic acid-treated or salicylic acid-deficient rice plants. In rice leaves, Δrbf1 inoculation caused necrosis and induced defense-related gene expression, which led to a higher level of diterpenoid phytoalexin accumulation than the wild-type fungus did. Δrbf1 showed unusual differentiation of IH and dispersal of the normally BIC-focused effectors around the short primary hypha and the first bulbous cell. In the Δrbf1-invaded cells, symplastic effectors were still translocated into rice cells but with a lower efficiency. These data indicate that RBF1 is a virulence gene essential for the focal BIC formation, which is critical for the rice blast fungus to suppress host immune responses.
• Development of a fluorescence-based mitotic reporter strain of M. oryzae that expresses GFP-NLS together with H1-tdTomato.
• M. oryzae is hypothesized to undergo semi-closed mitosis accompanied by closure of septal pores. • A nucleus undergoes extreme constriction and elongation during migration through the narrow invasive hyphal peg.
To study nuclear dynamics of Magnaporthe oryzae, we developed a novel mitotic reporter strain with GFP-NLS (localized in nuclei during interphase but in the cytoplasm during mitosis) and H1-tdTomato (localized in nuclei throughout the cell cycle). Time-lapse confocal microscopy of the reporter strain during host cell invasion provided several new insights into nuclear division and migration in M. oryzae: (i) mitosis lasts about 5 min; (ii) mitosis is semi-closed; (iii) septal pores are closed during mitosis; and (iv) a nucleus exhibits extreme constriction (approximately from 2 μm to 0.5 μm), elongation (over 5 μm), and long migration (over 16 μm). Our observations raise new questions about mechanisms controlling the mitotic dynamics, and the answers to these questions may result in new means to prevent fungal proliferation without negatively affecting the host cell cycle.
Hemibiotrophic pathogens are some of the most destructive plant pathogens, causing huge economic losses and threatening global food security. Infection with these organisms often involves an initial biotrophic infection phase, during which the pathogen spreads in host tissue asymptomatically, followed by a necrotrophic phase, during which host-cell death is induced. How hemibiotrophic pathogens trigger host necrosis and how plants inhibit the transition from the biotrophic stage to the necrotrophic stage in disease symptom expression are mainly unknown. The rice blast fungus Magnaporthe oryzae spreads in rice biotrophically early during infection, but this biotrophic stage is followed by a pronounced switch to cell death and lesion formation. Here, we show that the M. oryzae effector AvrPiz-t interacts with the bZIP-type transcription factor APIP5 in the cytoplasm and suppresses its transcriptional activity and protein accumulation at the necrotrophic stage. Silencing of APIP5 in transgenic rice leads to cell death, and the phenotype is enhanced by the expression of AvrPiz-t. Conversely, Piz-t interacts with and stabilizes APIP5 to prevent necrosis at the necrotrophic stage. At the same time, APIP5 is essential for Piz-t stability. These results demonstrate a novel mechanism for the suppression of effector-triggered necrosis at the necrotrophic stage by an NLR receptor in plants.
Plants have evolved hundreds of nucleotide-binding and leucine-rich domain proteins (NLRs) as potential intracellular immune receptors, but the evolutionary mechanism leading to the ability to recognize specific pathogen effectors is elusive.
Here, we cloned Pvr4 (a Potyvirus resistance gene in Capsicum annuum) and Tsw (a Tomato spotted wilt virus resistance gene in Capsicum chinense) via a genome-based approach using independent segregating populations.
The genes both encode typical NLRs and are located at the same locus on pepper chromosome 10. Despite the fact that these two genes recognize completely different viral effectors, the genomic structures and coding sequences of the two genes are strikingly similar. Phylogenetic studies revealed that these two immune receptors diverged from a progenitor gene of a common ancestor.
Our results suggest that sequence variations caused by gene duplication and neofunctionalization may underlie the evolution of the ability to specifically recognize different effectors. These findings thereby provide insight into the divergent evolution of plant immune receptors.
Recent evidence suggests that the ubiquitin-proteasome system (UPS) is involved in several aspects of plant immunity and a range of plant pathogens subvert the UPS to enhance their virulence. Here we show that proteasome activity is strongly induced during basal defense in Arabidopsis. Mutant lines of the proteasome subunits RPT2a and RPN12a support increased bacterial growth of virulent Pseudomonas syringae pv. tomato DC3000 (Pst) and Pseudomonas syringae pv. maculicola ES4326. Both proteasome subunits are required for Pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI) responses. Analysis of bacterial growth after a secondary infection of systemic leaves revealed that the establishment of systemic-acquired resistance (SAR) is impaired in proteasome mutants, suggesting that the proteasome also plays an important role in defense priming and SAR. In addition, we show that Pst inhibits proteasome activity in a type-III secretion dependent manner. A screen for type-III effector proteins from Pst for their ability to interfere with proteasome activity revealed HopM1, HopAO1, HopA1 and HopG1 as putative proteasome inhibitors. Biochemical characterization of HopM1 by mass-spectrometry indicates that HopM1 interacts with several E3 ubiquitin ligases and proteasome subunits. This supports the hypothesis that HopM1 associates with the proteasome leading to its inhibition. Thus, the proteasome is an essential component of PTI and SAR, which is targeted by multiple bacterial effectors.
Pseudomonas syringae pv. tomato DC3000 (PtoDC3000) is an extracellular model plant pathogen, yet its potential to produce secreted effectors that manipulate the apoplast has been under investigated. Here we identified 131 candidate small, secreted, non-annotated proteins from the PtoDC3000 genome, most of which are common to Pseudomonas species and potentially expressed during apoplastic colonization. We produced 43 of these proteins through a custom-made gateway-compatible expression system for extracellular bacterial proteins, and screened them for their ability to inhibit the secreted immune protease C14 of tomato using competitive activity-based protein profiling. This screen revealed C14-inhibiting protein-1 (Cip1), which contains motifs of the chagasin-like protease inhibitors. Cip1 mutants are less virulent on tomato, demonstrating the importance of this effector in apoplastic immunity. Cip1 also inhibits immune protease Pip1, which is known to suppress PtoDC3000 infection, but has a lower affinity for its close homolog Rcr3, explaining why this protein is not recognized in tomato plants carrying the Cf-2 resistance gene, which uses Rcr3 as a co-receptor to detect pathogen-derived protease inhibitors. Thus, this approach uncovered a protease inhibitor of P. syringae, indicating that also P. syringae secretes effectors that selectively target apoplastic host proteases of tomato, similar to tomato pathogenic fungi, oomycetes and nematodes.
The plant tumor disease known as crown gall was not called by that name until more recent times. Galls on plants were described by Malpighi (1679) who believed that these extraordinary growth are spontaneously produced. Agrobacterium was first isolated from tumors in 1897 by Fridiano Cavara in Napoli, Italy. After this bacterium was recognized to be the cause of crown gall disease, questions were raised on the mechanism by which it caused tumors on a variety of plants. Numerous very detailed studies led to the identification of Agrobacterium tumefaciens as the causal bacterium that cleverly transferred a genetic principle to plant host cells and integrated it into their chromosomes. Such studies have led to a variety of sophisticated mechanisms used by this organism to aid in its survival against competing microorganisms. Knowledge gained from these fundamental discoveries has opened many avenues for researchers to examine their primary organisms of study for similar mechanisms of pathogenesis in both plants and animals. These discoveries also advanced the genetic engineering of domesticated plants for improved food and fiber.
If I google “mealybugs,” the first pages of results deal almost entirely with ways of spotting and destroying them. There’s good reason for that: these small, sap-sucking bugs drain fluids from plants, spread diseases, foster the growth of molds, and cost millions in damage to crop growers every year. They destroy the things we eat, and so we destroy them.
But mealybugs are more than just symbols of both famine and pestilence. Over the last 15 years, a small team of scientists has shown that they are also symbols of interconnectedness. They are among the most spectacular examples of symbiosis—the phenomenon where different species live together in intimate association. And with every new discovery, their biology becomes even more elaborate and unbelievable.
The prelude to this story begins in the early 20th century, when an exceptionally productive zoologist named Paul Buchner started dissecting his way through the insect world. He showed that countless species are filled with microbes, many of which live inside their very cells. The mealybugs were no exception—they also contained inner bacteria, which seemed to be thickly embedded within “roundish or longish mucilaginous globules.” That is: big balls of mucus.
Buchner didn’t press the matter further. But when other scientists later analyzed these globules, they started getting very odd results. If the mealybugs swallowed antibiotics, the globules would rupture along with the bacteria inside them. Peculiar. The mucus also seemed to contain many of the elements of an actual cell. Also peculiar. And genetic studies showed that they contained DNA from two separate lineages of bacteria. That, at least, was explicable: Buchner’s globules probably contained two types of symbiotic bacteria rather than one.
In 2001, Carol von Dohlen tested this idea by studying the citrus mealybug—a tiny insect that looked like a lozenge dipped in icing sugar. Von Dohlen fashioned two fluorescent molecules—one red and one blue—that would each stick to DNA from one of the two bacteria. If the two microbes did indeed share the same living quarters, their respective glows should have blended into a sea of purple.
That is not what happened. Instead, von Dohlen saw red dots against a blue background. The red probe had stuck to the bacteria in the globules. But the blue probe was sticking to the globules themselves. These mucus-filled spheres weren’t enclosing two kinds of bacteria. They were bacteria.
Von Dohlen had discovered that the citrus mealybug is a living Russian doll—or perhaps a microbial turducken. The bacteria living in its cells have more bacteria living inside them. It contains multitudes, and its multitudes contain more multitudes. The bigger microbe was eventually named Tremblaya, and its inner companion was called Moranella. And then things got even weirder.
In 2011, von Dohlen teamed up with geneticist John McCutcheon to sequence the genomes of the two microbes. Both were very small, as is often the case with bacteria that find their way into insect cells. In the cozy confines of their hosts, these microbes can afford to lose genes that they would normally need for an independent existence. Tremblaya has even lost a group of supposedly indispensable genes that were there in the last common ancestor of all living things, and are found in everything from bacteria to bats. There should be twenty of them, and Tremblaya has none. It survives because the insect around it and the Moranella within it compensate for its genetic shortfall.
This convoluted set-up developed gradually. Tremblaya was first of the two partners to colonize mealybugs: it’s there in all the species from one particular lineage, and there are some mealybugs that carry it and it alone. Snug in a bug, it began jettisoning genes. In the citrus mealybug, Moranella joined the partnership. The duo became a trio, and Tremblaya continued its slide into genetic pauperdom. As long as any gene exists in one of the partners, the others can afford to lose it.
That’s abundantly clear when you look at genes for making nutrients. For example, it takes nine genes to make an essential amino acid called phenylalanine. But none of the three partners makes all nine. Tremblaya can build 1, 2, 5, 6, 7 and 8; Moranella can make 3, 4, and 5; and the mealybug alone makes the 9th. As I wrote in my new book, this reminds me of the Graeae of Greek mythology: the three sisters who share one eye and one tooth between them. They are still distinct entities, but they’re each like thirds of a single whole. They cooperate to make nutrients that they all rely upon, and none can survive without the other.
Now things get really strange. Other species of mealybugs are also Russian dolls, with the same bug-in-a-bug-in-a-bug set-up. One of them—the long-tailed mealybug—even seems to have two kinds of inner bacteria living inside its outer one.
No matter the mealybug species, the outer bacterium is always Tremblaya. But the inner bacterium varies considerably—it’s Moranella in the citrus mealybug, but different microbes in the other insects. The most obvious explanation for this pattern is that some ancestral mealybug became infected with its two nested microbes. As the insects diverged into different species, so did the microbes within them. For whatever reason, the outer one stayed the same, while the inner one changed into new forms—Moranella being just one of them. “It’s so weird and so uncommon to get these bacteria inside of each other that I thought it had to happen once,” says McCutcheon.
Parasitic plants in the Orobanchaceae cause serious agricultural problems worldwide. Parasitic plants develop a multicellular infectious organ called a haustorium after recognition of host-released signals. To understand the molecular events associated with host signal perception and haustorium development, we identified differentially regulated genes expressed during early haustorium development in the facultative parasite Phtheirospermum japonicumusing a de novo assembled transcriptome and a customized microarray. Among the genes that were upregulated during early haustorium development, we identified YUC3, which encodes a functional YUCCA (YUC) flavin monooxygenase involved in auxin biosynthesis. YUC3 was specifically expressed in the epidermal cells around the host contact site at an early time point in haustorium formation. The spatio-temporal expression patterns of YUC3 coincided with those of the auxin response marker DR5, suggesting generation of auxin response maxima at the haustorium apex. Roots transformed with YUC3 knockdown constructs formed haustoria less frequently than nontransgenic roots. Moreover, ectopic expression of YUC3 at the root epidermal cells induced the formation of haustorium-like structures in transgenic P. japonicum roots. Our results suggest that expression of the auxin biosynthesis gene YUC3 at the epidermal cells near the contact site plays a pivotal role in haustorium formation in the root parasitic plant P. japonicum.
For over 140 years, lichens have been regarded as a symbiosis between a single fungus, usually an ascomycete, and a photosynthesizing partner. Other fungi have long been known to occur as occasional parasites or endophytes, but the one lichen–one fungus paradigm has seldom been questioned. Here we show that many common lichens are composed of the known ascomycete, the photosynthesizing partner, and, unexpectedly, specific basidiomycete yeasts. These yeasts are embedded in the cortex, and their abundance correlates with previously unexplained variations in phenotype. Basidiomycete lineages maintain close associations with specific lichen species over large geographical distances and have been found on six continents. The structurally important lichen cortex, long treated as a zone of differentiated ascomycete cells, appears to consistently contain two unrelated fungi.
It’s the ancient story of plant evolution: photosynthetic algae moved to damp places on land, eventually evolving more complex architecture, and spreading across almost all terrestrial habitats. To cope with the drier conditions, plants developed roots to absorb water, and vascular tissue to transport it; a waxy cuticle coating their surfaces to prevent evaporation; and microscopic pores called stomata that open to allow carbon dioxide to diffuse in for photosynthesis but close to prevent excessive water loss.
How, then, does eelgrass (Zostera marina) fit in to this tale? It’s a monocot descended from the flowering plants, but it has turned its back on dry land and returned to the sea; a rare feat that only appears to have happened on three occasions. The recent sequencing of the eelgrass genome has revealed several interesting insights into the dramatic genetic changes that have allowed it to adapt to what lead author Professor Jeanine Olsen described as, “arguably the most extreme adaptation a terrestrial (and even a freshwater) species can undergo.”
Sayonara to stomata
If you live in the sea, conserving water isn’t your main concern. Eelgrass was known to lack stomata, but genetic comparisons to other species, including its freshwater relative Spirodela polyrhiza, revealed the first surprise of the study: eelgrass has lost not only its stomata but also the genes involved in their development and patterning. “The genes have just gone, so there’s no way back to land for seagrass,” said Olsen.
A difference in defense
When angiosperms are attacked by herbivores or pathogens, their defense response typically involves the release of volatile secondary metabolites through their stomata. How can eelgrass release these compounds without stomata? The answer is: it doesn’t. The genome study found that eelgrass is missing crucial genes involved in making ethylene (an important hormone release in times of stress), as well as those responsible for producing non-metabolic terpenoids, which act to repel pests.
Selective pressures of the marine environment differ greatly from those of terrestrial habitats, so different pathways may be involved. Second, eelgrass has a wide repertoire of pathogen resistance genes, which suggests that it is exposed to a very different set of pathogens that may not respond to typical immune responses. Third, volatile secondary metabolites are often involved in attracting pollinators; this is not believed to be necessary in eelgrass, where submarine pollination occurs using the water itself.
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