Seminars in cell & developmental biology最新文献

Oomycete plant pathogens, such as Phytophthora and Pythium species produce motile dispersal agents called zoospores that actively target host plants. Zoospores are exceptional in their ability to display taxis to chemical, electrical and physical cues to navigate the phyllosphere and reach stomata, wound sites and roots. Many components of root exudates have been shown attractive or repulsive to zoospores. Although some components possess very strong attractiveness, it seems that especially the mix of components exuded by the primary host is most attractive to zoospores. Zoospores actively approach attractants with swimming behaviour reminiscent of other microswimmers. To achieve a unified description of zoospore behaviour when sensing an attractant, we propose the following terms for the successive stages of the homing response: reorientation, approaching, retention and settling. How zoospores sense and process attractants is poorly understood but likely involves signal perception via cell surface receptors. Since zoospores are important for infection, undermining their activity by luring attractants or blocking receptors seem promising strategies for disease control.

Downy mildews are obligate oomycete pathogens that attack a wide range of plants and can cause significant economic impacts on commercial crops and ornamental plants. Traditionally, downy mildew disease control relied on an integrated strategies, that incorporate cultural practices, deployment of resistant cultivars, crop rotation, application of contact and systemic pesticides, and biopesticides. Recent advances in genomics provided data that significantly advanced understanding of downy mildew evolution, taxonomy and classification. In addition, downy mildew genomics also revealed that these obligate oomycetes have reduced numbers of virulence factor genes in comparison to hemibiotrophic and necrotrophic oomycetes. However, downy mildews do deploy significant arrays of virulence proteins, including so-called RXLR proteins that promote virulence or are recognized as avirulence factors. Pathogenomics are being applied to downy mildew population studies to determine the genetic diversity within the downy mildew populations and manage disease by selection of appropriate varieties and management strategies. Genome editing technologies have been used to manipulate host disease susceptibility genes in different plants including grapevine and sweet basil and thereby provide new soucres of resistance genes against downy mildews. Previously, it has proved difficult to transform and manipulate downy mildews because of their obligate lifestyle. However, recent exploitation of RNA interference machinery through Host-Induced Gene Silencing (HIGS) and Spray-Induced Gene Silencing (SIGS) indicate that functional genomics in downy mildews is now possible. Altogether, these breakthrough technologies and attendant fundamental understanding will advance our ability to mitigate downy mildew diseases.

Plant diseases caused by soilborne pathogens are a major limiting factor in crop production. Bacterial wilt disease, caused by soilborne bacteria in the Ralstonia solanacearum Species Complex (Ralstonia), results in significant crop loss throughout the world. Ralstonia invades root systems and colonizes plant xylem, changing plant physiology and ultimately causing plant wilting in susceptible varieties. Elucidating how Ralstonia invades and colonizes plants is central to developing strategies for crop protection. Here we review Ralstonia pathogenesis from root detection and attachment, early root colonization, xylem invasion and subsequent wilting. We focus primarily on studies in tomato from the last 5–10 years. Recent work has identified elegant mechanisms Ralstonia uses to adapt to the plant xylem, and has discovered new genes that function in Ralstonia fitness in planta. A picture is emerging of an amazingly versatile pathogen that uses multiple strategies to make its surrounding environment more hospitable and can adapt to new environments.

Regulation of protein synthesis is a strong determinant of potyviral pathogenicity. The Potyviridae family is the largest family of plant-infecting positive sense RNA viruses. Similar to the animal-infecting Picornaviridae family, the potyviral RNA genome lacks a 5′ cap, and instead has a viral protein (VPg) linked to its 5′ end. Potyviral genomes are mainly translated into one large polyprotein relying on a single translation event to express all their protein repertoire. In the absence of the 5′ cap, the Potyviridae family depends on cis-acting elements in their 5′ untranslated regions (UTR) to recruit the translation machinery. In this review, we summarize the diverse 5′UTR-driven, cap-independent translation mechanisms employed by the Potyviridae family including scanning-dependent mechanism, internal initiation, and the stimulatory role of the VPg. These mechanisms have direct implications on potyviral pathogenicity, including host range specificity and resistance. Finally, we discuss how these viral strategies could not only inform new avenues for engineering and/or breeding for crop resistance but would also provide opportunities for the development of biotechnological tools for large-scale protein production in plant systems.

Plasmodiophora brassicae Wor., the clubroot pathogen, is the perfect example of an “atypical” plant pathogen. This soil-borne protist and obligate biotrophic parasite infects the roots of cruciferous crops, inducing galls or clubs that lead to wilting, loss of productivity, and plant death. Unlike many other agriculturally relevant pathosystems, research into the molecular mechanisms that underlie clubroot disease and Plasmodiophora-host interactions is limited. After release of the first P. brassicae genome sequence and subsequent availability of transcriptomic data, the clubroot research community have implicated the involvement of phytohormones during the clubroot pathogen’s manipulation of host development. Herein we review the main events leading to the formation of root galls and describe how modulation of select phytohormones may be key to modulating development of the plant host to the benefit of the pathogen. Effector-host interactions are at the base of different strategies employed by pathogens to hijack plant cellular processes. This is how we suspect the clubroot pathogen hijacks host plant metabolism and development to induce nutrient-sink roots galls, emphasizing a need to deepen our understanding of this master manipulator.

Pectobacterium and Dickeya species belonging to the Soft Rot Pectobacteriaceae (SRP) are one of the most devastating phytopathogens. They degrade plant tissues by producing an arsenal of plant cell wall degrading enzymes. However, SRP-plant interactions are not restricted to the production of these “brute force” weapons. Additionally, these bacteria apply stealth behavior related to (1) manipulation of the host plant via induction of susceptible responses and (2) formation of heterogeneous populations with functionally specialized cells. Our review aims to summarize current knowledge on SRP-induced plant susceptible responses and on the heterogeneity of SRP populations. The review shows that SRP are capable of adjusting the host's hormonal balance, inducing host-mediated plant cell wall modification, promoting iron assimilation by the host, stimulating the accumulation of reactive oxygen species and host cell death, and activating the synthesis of secondary metabolites that are ineffective in limiting disease progression. By this means, SRP facilitate host plant susceptibility. During host colonization, SRP populations produce various functionally specialized cells adapted for enhanced virulence, increased resistance, motility, vegetative growth, or colonization of the vascular system. This enables SRP to perform self-contradictory tasks, which benefits a population's overall fitness in various environments, including host plants. Such stealthy tactical actions facilitate plant-SRP interactions and disease progression.

Understanding the mechanism by which cells coordinate their differentiation and migration is critical to our understanding of many fundamental processes such as wound healing, disease progression, and developmental biology. Mathematical models have been an essential tool for testing and developing our understanding, such as models of cells as soft spherical particles, reaction-diffusion systems that couple cell movement to environmental factors, and multi-scale multi-physics simulations that combine bottom-up rule-based models with continuum laws. However, mathematical models can often be loosely related to data or have so many parameters that model behaviour is weakly constrained. Recent methods in machine learning introduce new means by which models can be derived and deployed. In this review, we discuss examples of mathematical models of aspects of developmental biology, such as cell migration, and how these models can be combined with these recent machine learning methods.

Epithelial cancer is the one of most lethal cancer type worldwide. Targeting the early stage of disease would allow dramatic improvements in the survival of cancer patients. The early stage of the disease is related to cancer cell spreading across surrounding healthy epithelium. Consequently, deeper insight into cell dynamics along the biointerface between epithelial and cancer (mesenchymal) cells is necessary in order to control the disease as soon as possible. Cell dynamics along this epithelial-cancer biointerface is the result of the interplay between various biological and physical mechanisms. Despite extensive research devoted to study cancer cell spreading across the epithelium, we still do not understand the physical mechanisms which influences the dynamics along the biointerface. These physical mechanisms are related to the interplay between physical parameters such as: (1) interfacial tension between cancer and epithelial subpopulations, (2) established interfacial tension gradients, (3) the bending rigidity of the biointerface and its impact on the interfacial tension, (4) surface tension of the subpopulations, (5) viscoelasticity caused by collective cell migration, and (6) cell residual stress accumulation. The main goal of this study is to review some of these physical parameters in the context of the epithelial/cancer biointerface elaborated on the model system such as the biointerface between breast epithelial MCF-10A cells and cancer MDA-MB-231 cells and then to incorporate these parameters into a new biophysical model that could describe the dynamics of the biointerface. We conclude by discussing three biophysical scenarios for cell dynamics along the biointerface, which can occur depending on the magnitude of the generated shear stress: a smooth biointerface, a slightly-perturbed biointerface and an intensively-perturbed biointerface in the context of the Kelvin-Helmholtz instability. These scenarios are related to the probability of cancer invasion.

Cancer invasion through the surrounding epithelium and extracellular matrix (ECM) is the one of the main characteristics of cancer progression. While significant effort has been made to predict cancer cells response under various drug therapies, much less attention has been paid to understand the physical interactions between cancer cells and their microenvironment, which are essential for cancer invasion. Considering these physical interactions on various co-cultured in vitro model systems by emphasizing the role of viscoelasticity, the tissue surface tension, solid stress, and their inter-relations is a prerequisite for establishing the main factors that influence cancer cell spread and develop an efficient strategy to suppress it. This review focuses on the role of viscoelasticity caused by collective cell migration (CCM) in the context of mono-cultured and co-cultured cancer systems, and on the modeling approaches aimed at reproducing and understanding these biological systems. In this context, we do not only review previously-published biophysics models for collective cell migration, but also propose new extensions of those models to include solid stress accumulated within the spheroid core region and cell residual stress accumulation caused by CCM.