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HIGHLIGHTS

The slow growth of the bacteria Xylella fastidiosa:

metabolic accident or epidemic strategy?

Xylella fastidiosa is a bacterium which causes many diseases affecting plants. It has preoccupied European agriculture since its emergence in Italy, where it caused the death of many olive trees. Better understanding how this bacteria works helps fight it. A collaboration between the Plant Microbes Environment Interactions Laboratory of INRAE ​​Occitanie-Toulouse and the Horticulture and Seeds Research Institute of INRAE ​​Pays de la Loire studied its metabolic network using systems biology and modeling tools . This work appeared in the American Society for Microbiology Journals mSystems.

                                                                                                      © Marie-Agnès Jacques, INRAE

How are this expansion and virulence possible when this pathogen has a growth described as fastidious because it is very slow?

So slow that it complicates its diagnosis in plants and its study in the laboratory. This physiological characteristic, shared with several pathogenic bacteria of man, seems paradoxical. This slow growth is an intrinsic characteristic of the organism. A research team from the Laboratory of Plant Microbes Environment Interactions (INRAE-CNRS) and researchers from the Horticulture and Seeds Research Institute of INRAE ​​in Angers, worked together to better understand the metabolism of this bacterium.

Using tools from systems biology and modeling, the researchers discovered that the metabolic network of Xylella fastidiosa is, unexpectedly, complete but reduced to its essentials. It has, for example, half as many reactions as the reference organism Escherichia Coli. Thus, the redundant pathways of metabolism have disappeared, especially those promoting rapid and efficient growth. The metabolic network of Xylella fastidiosa is therefore inefficient and fragile. The synthesis of exopolysaccharide, one of its virulence factors, has also been shown to be ineffective, even becoming a burden for growth.

A weakness that becomes a strength

It seems that this fastidious growth results from an evolution of this pathogenic agent, undoubtedly allowing it to escape the mechanisms of detection and defense of the plants. Strategy which seems to be winning, in view of the increasing dissemination of Xylella fastidiosa in the world.

To better understand the metabolism of Xylella fastidiosa, work is continuing with the study of several genes in order to understand their involvement in fastidious growth.

Scientists are trying to better understand how this slow growth affects the spread of the bacteria in host plants. All these advances are necessary to better fight against the bacteria.

 


Gerlin L, Cottret L, Cesbron S, Taghouti G, Jacques MA, Genin S, Baroukh C. 2020. Genome-scale investigation of the metabolic determinants generating bacterial fastidious growth. ASM Journals, mSystems Vol. 5, No. 2 : e00698-19.

https://doi.org/10.1128/mSystems.00698-19

The slow growth of the bacterium Xylella fastidiosa: metabolic accident or epidemic strategy? | INRAE ​​INSTIT

Polygale à feuille de myrte infectée par Xylella fastidiosa (sous-espèce multiplex). Les symptômes visibles sont le jaunissement et dessèchement des feuilles. Xylella fastidiosa peut entrainer la mort de la plante.

Cooperation within the fungal network allows Sclerotinia to diversify its victims

 

Common grounds for quantitative disease resistance

When a parasite gains the ability to infect new hosts, terrible epidemics can occur, as in the case of COVID-19. The fungus responsible for white rot is naturally capable of infecting hundreds of plant species belonging to very diverse botanical families. INRAE researchers from the Laboratoire des Interactions Plantes Microbes Environnement (LIPME) in Toulouse wanted to know how plants as different as beet and bean react to the attack of this fungus at the molecular level. This study published in the journal The Plant Cell revealed the diversity of mechanisms that plants have to slow down the progression of the infection.

A frequent and durable form of immunity in plants

Some plant pathogens actively kill the cells of their hosts to cause disease. In response, plants have developed dedicated resistance mechanisms such as quantitative disease resistance (QDR). Studies on QDR have so far shown that this form of immunity is common in nature and relatively durable. The fungus Sclerotinia sclerotiorum causes white rot diseases on plant species from a wide range of botanical families, such as bean, castor bean, thalecress, tomato, sunflower and beet. What is the diversity of transcriptional responses to S. sclerotiorum in these plants? Are genes that are highly regulated during infection conserved or rather specific on each plant species?

Identical resistance genes in several plant species

The LIPME researchers showed in their study that a majority of the genes involved is conserved across botanical families, but genes are not always activated with the same intensity. This finding provides a better understanding of how plant evolution has shaped their response to pests and invites the use of gene expression to identify disease resistance mechanisms operating in many plant species.

The researchers identified the repertoire of conserved genes that respond similarly to fungal infection across botanical families. This resource will enable future searches for quantitative resistance genes active in multiple plant species. Future studies will focus on the molecular and evolutionary mechanisms underlying interspecific expression variation of QDR genes.

 

 

 

 

 

 

 

 

Rémi Peyraud , Malick Mbengue , Adelin Barbacci , Sylvain Raffaele Intercellular cooperation in a fungal plant pathogen facilitates host colonization. . 2019 Feb 19; 116 (8): 3193-3201. Proc Natl Acad Sci US A.

DOI: 10.1073 / pnas.1811267116

Advances on plant-pathogen interactions from molecular toward systems biology perspectives.

Peyraud R, Dubiella U, Barbacci A, Genin S, Raffaele S, Roby D. Plant J. 2017 May; 90 (4): 720-737.

doi: 10.1111 / tpj.13429. Epub 2017 Feb 10.

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When a bacterium repairs its damaged DNA to adapt to its environment


DNA is subjected to numerous physicochemical constraints of intracellular or extracellular origin, which lead to the regular appearance of lesions, including DNA breaks. Faced with this, bacteria develop repair strategies which can have surprising consequences on the bacteria's ability to adapt to their environment. This is what researchers from the Laboratory of Interactions-Plants-Microorganisms, LIPM (INRAE-CNRS) showed in an article published on December 04, 2018 in the journal Nucleic Acids Research.

DNA (deoxyribonucleic acid), a biological macromolecule constituting chromosomes, is formed from the linear sequence of several million / billion nucleotides, the nature and very precise order of which determine the genetic information of living beings. Maintaining the integrity of this molecule is therefore a priority for living beings to ensure the expression and faithful transmission of their genetic heritage. At the level of a cell, the slightest chromosome break, if it is not repaired, can have irreversible consequences, including the death of the cell.

How does a bacterium adapt to its environment?


Living beings have therefore developed mechanisms for repairing DNA breaks, one of which, called NHEJ (for Non-Homologous End-Joining) consists of bringing together and "re-gluing" the ends of DNA, restoring thus the integrity of the molecule.

Unlike other more faithful repair mechanisms, NHEJ repairs chromosomes sometimes at the cost of "tinkering" at the repair junction, which can lead to a modification of the local nucleotide composition and therefore sometimes to a change. the meaning of genetic information (we speak of mutations).

An outstanding DNA repairer

By studying the NHEJ repair mechanism in a soil bacterium, Sinorhizobium meliloti, two surprising observations were made:

  • The ability of bacteria to repair NHEJ breaks increases under stressful environmental conditions, such as when ambient temperature rises.

  • On the other hand, among the “tinkering” of the NHEJ repair system, it can happen to accidentally integrate a DNA fragment of foreign origin at the level of the repaired break.

These observations made in the laboratory could find an echo in nature: when bacteria are in unfavorable environmental conditions, the increase in their DNA repair capacity by NHEJ would lead to an increase in the frequency of appearance of mutations in their cells. genome. In addition, stimulating their ability to integrate foreign DNA would make it easier for them to acquire genetic information from other organisms (this is referred to as "horizontal gene transfer").

These mechanisms, present in many bacterial species, could thus allow them to increase their potential for genetic evolution, and therefore their ability to adapt to new environmental conditions.

This work was carried out within the Laboratory of Plants-Microorganisms Interactions ( LIPM ), and was supported by INRAE ​​through a young scientist contract with Pierre Dupuy, and funding from the Department of Plant Health and Environment.

                                                                                                                                                                             

                                                                                                                                                                             

 

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Dupuy, P., Sauviac, L., and Bruand, C. Stress-inducible NHEJ in bacteria: function in DNA repair and acquisition of heterologous DNA. Nucleic Acids Research, 2018 Dec 4. https://doi.org/10.1093/nar/gky1212


https://www.inrae.fr/actualites/quand-bacterie-repare-son-adn-endommage-sadapter-son-environnement

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