180 Papers found (0.012 seconds)

Becker, S.F. et al. (2019) International Worm Meeting "You are what you experience : The impact of environnment on transdifferentiation."

Morin, M. - C., Jarriault, S., Medina Sanchez, J.D., Becker, S.F.

[

International Worm Meeting,

2019]

Purpose: The balance between cellular identity maintenance and cellular plasticity (as the potential to change identity on a functional and morphological level) is a major challenge for organismal tissues. Uncontrolled cell fate changes can cause dysfunctional cellular behaviors such as cancer. Unraveling the mechanisms behind cell type conversion will further help to develop a safe environment for regenerative medicine. Here, we describe how chromatin remodeling as well as several external factors impacts on cellular identity and increase a cell's plasticity potential. Methods: We use a natural cell identity conversion in the worm to determine how a cell can change or maintain its identity. C. elegans rectal to neuronal Y-to-PDA transition is a bona fide robust transdifferentiation (Td) event: During L2 larval stage the rectal identity of the Y cell is erased completely, followed by redifferentiation into a fully functional motoneuron, named PDA. Results: We previously described a subset of essential factors driving Td initiation. We identified two novel positive regulators of Td: lin-15A and lin-56. In null mutants for these genes, PDA neurons are not made and Y cells remain epithelial. Genetic interactions suggest that these two genes act in a parallel pathway to the previously described "drivers" during Td initiation and that they antagonize a SynMuvB-based identity maintenance mechanism to "license" Td in the Y cell. Our data suggest that this brake is represented by a defined chromatin state, and genetic alterations of chromatin architecture are able to suppress lin-15A phenotype. Excitingly, we found that this suppression is phenocopied under different environmental conditions: in particular, starvation and caloric restriction decrease PDA defects. Our data point to a food signal mediated by IIS and TOR pathways impacting cellular plasticity. Conclusion: Our data suggest that Td initiation requires not only drivers TF but also "licensers" such as lin-15A and lin-56 that allow Td to occur by removing negative regulators and enabling chromatin remodelling, whereas several environmental conditions can bypass the need for the licensers, and thus, increase plasticity and allow transdifferentiation to occur.

Valeria Pavet et al. (2008) European Worm Meeting "Deciphering epithelial cell plasticity in C. elegans"

Iva Greenwald, Nadege Vaucamps, Sophie JARRIAULT, Valeria Pavet, Yannick Schwab

[

European Worm Meeting,

2008]

Understanding how a differentiated cell is able to change its identity. and give rise to a different kind of differentiated cell - process called. transdifferentiation (or TD)- is a challenging task, and the results. obtained will have a profound impact in both basic and clinical science.. In C. elegans, an epithelial cell named "Y" is born in the embryo and is. one of the six epithelial cells that form the rectum in a young larva.. During the second larval stage, Y detaches from the rectum, migrates. anteriorly and becomes a motor-neuron named "PDA", without cell division.. We have shown that the Y-to-PDA conversion represents a bona fide TD. event. Indeed, we have demonstrated that Y presents exclusively. epithelial features while being a part of the rectum, and that these. characteristics are lost and replaced by purely neuronal ones after its. TD into PDA. We have performed an initial characterization of this. process, using genetics and cell ablation to explore factors pertaining. to competence, lineage, and local environment. We found that. transdifferentiation does not depend on fusion with a neighbouring cell. or require migration of Y away from the rectum; that other rectal. epithelial cells are not competent to transdifferentiate; and that. transdifferentiation requires the EGL-5 and SEM-4 transcription factors. and LIN-12/Notch signalling. In order to identify and characterize the. genes and the genetic cascade(s) involved in each step of the Y-to-PDA. TD, we have performed a forward genetic screen for mutants that do not. have a PDA neuron. The mutants obtained fall into two clearly. distinguishable morphological classes: mutants having a persistent. epithelial Y cell that did not transdifferentiate and mutants where an. epithelial Y cell is no longer recognizable. We have started to map and. characterize mutants belonging to the two morphological groups and use. them to examine the intermediate steps of TD. We believe that this system. will allow us to identify the mechanisms underlying this TD event and to. propose a model of how cell plasticity proceeds.

Ahier, A. et al. (2011) International Worm Meeting "EGL-27/MTA1 interacts with SEM-4/SALL and other pluripotency factors to potentiate the Y-to-PDA cell reprogramming event."

Ahier, A., Kagias, K., Jarriault, S., Fischer, N.

[

International Worm Meeting,

2011]

The cell plasticity describes the ability for a differentiated cell to be reprogrammed and adopt another identity. When the final identity is also differentiated, this phenomenon is called transdifferentiation (TD). We recently characterized such an event in Caenorhabditis elegans, in which an epithelial rectal cell (Y) switches to a neuronal cell (PDA) during the L2-L3 larval stages transition (Jarriault et al, 2008). This phenomenon occurs as a multistep process in which the Y cell, and not its neighbours, first acquires the competence to change its identity, initiates the TD process and transits through discrete non-pluripotent steps before adopting the PDA identity (Richard et al, 2011). Here, we have focused on the TD initiation and addressed the role of factors involved in chromatin remodeling. Indeed, many evidences point to a role of chromatin factors in the maintenance of cell identity memory and gene expression regulation. Moreover chromatin structure appears to be widely remodeled during reprogramming events. Through a targeted RNAi screen for factors impacting on chromatin modifications, we identified egl-27, an homologue of the human MTA1, a NuRD (Nucleosome Remodeling and Deacetylase complex) component, as a key player in this process. In absence of egl-27/mta1 activity, the Y cell is unable to change its identity and no TD is initiated, suggestive of a lack of competence. Interestingly, mta-1 is necessary for the maintenance of ES cells pluripotency in mammals. Investigation of potential interactors for egl-27/mta1, using RNAi and/or corresponding mutant analysis, revealed the implication of another conserved nuclear factor previously described in the initiation of Y TD: sem-4/sall. This is an exciting partner, as SEM-4/SALL is important for ES cells pluripotency and enhances IPS reprogramming. Furthermore, conventional biochemical approaches allowed us to show that EGL-27 physically interacts with SEM-4/SALL and other conserved pluripotency factors. Thus, EGL-27/MTA1 and SEM-4/SALL appear to be components of a conserved cell plasticity complex which is necessary to allow the Y cell to be reprogrammed. Our data highlight a new function for these ES cell factors for the first time in a natural TD event, in vivo, and suggest that common mechanisms may be at play between different cell plasticity phenomena. The determination of the molecular mechanisms allowing a cell to be plastic has significant implications on our ability to better and safely reprogram cells for regenerative medicine purposes.

Larson, E. M. et al. (2015) International Worm Meeting "Pilot studies to determine if dietary polyunsaturated fatty acids cause sterility in plant-parasitic nematodes."

Dinh, P. T. Y., Elling, A. A., Larson, E. M., Watts, J. L., Davies, L. J.

[

International Worm Meeting,

2015]

Plant parasitic nematodes are one of the major pests affecting agricultural crops. Root-knot nematodes (RKNs) are among the most damaging group of plant parasitic nematodes. These nematodes are obligate parasites that infect their hosts in the root system. These parasites lead to a loss in excess of $100 billion for farmers due to reduced crop yield. Currently, the means of control for plant parasitic nematodes are chemical pesticides and resistant cultivars. However, many of the chemicals have been banned due to health concerns and certain populations of the nematodes have been able to overcome the resistance in selectively bred cultivars. As a result, a new method of control needs to be developed. We previously showed that when Caenorhabditis elegans are cultured on media containing specific polyunsaturated fatty acids (PUFAs) they become sterile. This led us to hypothesize that if plant parasitic nematodes are exposed to these particular PUFAs, they will display a reduction in the production of offspring. We obtained transgenic Arabidopsis plants expressing a specific PUFA and are currently conducting experiments to determine if this PUFA can reduce infection rates and reduce fertility of the root knot nematode Meloidogyne incognita. This represents a novel technique for controlling plant parasitic nematodes. .

Michael S. Voegtline et al. (2007) International Worm Meeting "Induced resistance against Meloidogyne incognita infection and egg production via transfection of modified Bacillus thurengiensis (Bt) crystal toxin genes and expression in tomato hairy roots."

Senait Bekele, Anderson Tan, Michael S. Voegtline, Xiang-qian Li, Raffi V. Aroian

[

International Worm Meeting,

2007]

To confer resistance against the root gall nematode Meloidogyne incognita, a study was performed to introduce Bacillus thuringiensis (Bt) crystal protein toxin genes into tomato plant (Lycopersicon esculentum var. Rutgers select) hairy roots. Crystal toxin gene sequences were altered to allow plant expression and in some cases also included unique intron sequences to aid in protein expression. Genes were inserted into the pBluscript in concert with a double 35S plant promoter and kanamycin resistance. The vector was used to transform the plant pathogenic bacterium Agrobacterium rhizogenes. The transformed Agrobacterium was used to induce the toxin genes into plants by co-cultivation with tomato cotyledons. Hairy root lines were selected via kanamycin resistance and once established, root extracts were tested for relative expression of crystal toxin by western blot analysis using a polyclonal detection sera specific for each toxin. Induced resistance against the root gall nematode was examined by hairy root challenge against a load of J2 stage parasitic nematodes. Subsequent enumeration of total egg masses (EM), total sites of infection (INF) and total calculated eggs (TE) per root plate were used to determine resistance against nematode infections. Results of these studies will be discussed. Data suggests that some Bt crystal proteins have excellent potential to control plant parasitic nematode (PPN) infections in transgenic plants.

DiGennaro, Peter et al. (2013) International Worm Meeting "Structure of a plant peptide hormone and a root-knot nematode-encoded mimic."

Scholl, Elizabeth, Imin, Nijat, Bobay, Benjamin, Mck. Bird, David, DiGennaro, Peter, Djordjevic, Michael

[

International Worm Meeting,

2013]

Root-knot nematodes (RKN; Meloidogyne spp.) are a pervasive pest of vascular plants and cause substantial crop loss worldwide. The molecular basis underpinning the intimate plant-nematode symbiosis remains arcane. As an obligate parasite that must execute complex behavior to reproduce, mutations that are trivial in C. elegans are lethal in RKN. Further, transformation remains elusive, and RNAi unpredictable. Yet although the genetic tool-kit is limited, emergent technologies have greatly aided the exploration the host-parasite interaction, and permit traditional genetic manipulation. Using a targeted computational approach, we identified multiple families of plant peptide hormone mimics encoded within the RKN genome. One family, C-terminal Encoded Peptide (CEP) has been implicated in the suppression of lateral roots and formation of galls, a hallmark of RKN pathology. RKN uniquely encode and express mimics of CEP during parasitism and RKN encoded CEP phenocopy endogenous hormones in bioassays. To better understand their role in the parasitic interaction, we used NMR to compare tertiary structures of plant and nematode encoded CEP hormones. In-solution models reveal family-specific structural properties that have been implicated in receptor binding. Molecular dynamic simulations demonstrated relative conformational plasticity of host CEP. This is consistent with promiscuous interaction with multiple receptors to regulate diverse pathways throughout the plant. In contrast, the comparatively rigid structure of RKN-encoded mimics likely reflects their function in a singular niche. These analyses implicate RKN-encoded plant peptide hormones as core communicative signals in the plant-nematode interaction and constitute a new methodological paradigm in studying effectors at the host-parasite interface.

Anderson H Tan et al. (2005) International Worm Meeting "Optimization of bioassay systems on plants expressing crystal toxin for the control of plant parasitic nematodes"

Raffi Aroian, Anderson H Tan, Xiang-qian Li

[

International Worm Meeting,

2005]

Every year, plant parasitic nematodes cause over $100 billion in damages due to crop loss and plant damage. Chemical pesticides are the most widespread form of PPN control, but with the prohibition of methyl bromide other approaches to control are necessary. One approach under consideration is Bacillus thuringiensis Bt Crystal (Cry) proteins. Crystal proteins produced by Bt have been commonly used for biocontrol of insects. Our lab has demonstrated that some Bt Cry proteins kill free-living nematodes and the free-living stages of one animal parasitic nematode (Nippostrongylus brasiliensis). These results then set the stage for testing whether Cry proteins can control plant-parasitic nematodes.Since most plant parasitic nematodes are obligate endoparasites that feed and develop inside the plant root, delivering Bt Cry protein requires the proteins be expressed directly in the plant. The Cry proteins would then transferred to the nematode through feeding.Our goal is to establish a reliable system for testing transgenic roots for control of endoparasitic nematodes. This involves expressing the proteins in an appropriate plant and/or root system, infecting those roots with an appropriate nematode host, and then quantitating various parameters of infection. We have synthesized plant-friendly versions of two of these toxins, Cry 6A and Cry 5B. These were transformed in tomato roots using Agrobacterum rhizogenes(hairy roots) and into Arabidopsis using A. tumefaciens. These plant systems are both candidates for infection by root-knot nematode, Meloidogyne incognita.We tested different growth media, lighting conditions, and inoculum levels, in order to optimize number of infections and to develop a reliable system to test the effect of Cry toxins on M. incognita. The experimental conditions and results will be presented.

Danchin, Etienne G.J. et al. (2014) Evolutionary Biology of Caenorhabditis and Other Nematodes "Contribution of horizontal gene transfers and duplications to genome evolution in plant-parasitic nematodes"

Abad, Pierre, Rancurel, Corinne, Danchin, Etienne G.J., Rosso, Marie-Noelle, Da Rocha, Martine

[

Evolutionary Biology of Caenorhabditis and Other Nematodes,

2014]

Horizontal gene transfer (HGT) is the transmission of genes by means other than direct inheritance from an ancestor to the offspring. HGT is accepted as a biologically and evolutionary significant phenomenon in bacteria but generally overlooked in animals. However, HGTs of biological importance have been suggested as soon as 1998 in nematodes with the identification of functional cellulases of bacterial origin in cyst nematodes. These secreted cellulases degrade cellulose, the main component of the plant cell wall and play an important role in these plant parasites. Initial analysis of the genome of the root-knot nematode Meloidogyne incognita revealed that as much as 60 genes from six different families encode plant cell wall-degrading enzymes and show highest similarity to bacterial genes. A similar repertoire was found in the genome of M. hapla, indicating that these genes have been acquired at least in a common ancestor of the two species. Using systematic phylogenetic analyses, we have shown that the most likely hypothesis for the presence of these gene families, otherwise generally absent in animals, was acquisition from bacteria via HGT followed by duplications. A survey of the literature allowed us to identify at least 12 different reported cases of HGT event in plant parasitic nematodes. Besides degradation of the plant cell wall, the corresponding gene products play important roles in other aspects of the parasitism such as modulation of plant defense, establishment of a feeding structure or nutrient metabolism. Recently, we have systematically scanned the genomes of the root-knot nematodes to identify genes potentially acquired via HGT. Using a combination of homology-based and phylogeny-based approaches, we have shown that at least 3.3 % of protein-coding genes are of foreign origin and were probably acquired via HGT. Hence, not only do HGT appear to have played an important role in the emergence of plant parasitism in nematodes but they also significantly contributed to the composition of the gene set itself. Thus, far from being negligible HGT appear as major evolutionary events in animals too. Interestingly, recent reports indicate that this phenomenon is not limited to nematode but also present in other animal lineages. Bdelloid rotifers currently hold the record with more than 8% of protein-coding genes possibly acquired via HGT of non animal origin.

Manohar, M. et al. (2019) International Worm Meeting "Nematode-derived metabolite ascr#18 mediates plant-nematode interactions."

Chen, S., Wang, X., Tenjo, F.J., Schroeder, F.C., Manohar, M., Klessig, D.F.

[

International Worm Meeting,

2019]

Plant-parasitic nematodes cause billions of dollars' worth of agricultural damage annually. Although resistant cultivars and nematicides have been used to control nematodes, there exists a need for more effective treatment strategies. Plants are known to respond to plant-parasitic nematodes similar to other pathogens; however, the underlying molecular mechanism remains elusive. Nematodes use molecules from a conserved pheromone family, the ascarosides, to regulate developmental and social behaviors. Previously, we have shown that ascr#18, the major ascaroside in the plant-parasitic nematodes, elicits plant defense response in monocots and dicots, improving their resistance to nematodes, bacterial and fungal pathogens. In recent work, we demonstrated that ascr#18 is taken up by Arabidopsis and tomato, metabolized into shorter side-chained ascarosides, and secreted into the rhizosphere via the roots. The identity of ascr#18 and metabolized ascarosides was confirmed by LC-MS/MS and using 13C-labeled derivatives. Since nematodes use peroxisomal ?-oxidation pathway to metabolize ascarosides, we investigated ascaroside metabolism in several Arabidopsis mutants defective in this pathway. Interestingly, a mutant defective in production of two acyl-CoA oxidases, acx1/acx5, is unable to metabolize ascr#18. In addition, we have shown that acx1/acx5 mutant is compromised in ascr#18-mediated enhanced resistance to root-knot nematodes. Our results suggest that plants use conserved metabolic pathways to process ascr#18 into its derivatives, thereby modifying the composition of their root exudates to regulate their interaction with nematodes

Skantar AM et al. (1997) International C. elegans Meeting "MOLECULAR GENETIC STUDIES OF DEVELOPMENTAL ARREST AND SEX DETERMINATION IN PLANT-PARASITIC NEMATODES"

Skantar AM, Bird DMcK, Conkling MA, Opperman CH

[

International C. elegans Meeting,

1997]

We are applying knowledge of selected C. elegans developmental pathways to understand plant-parasitic nematode life-cycles. We are interested in identifying the genes controlling developmental arrest, which occurs at the preparasitic L2 stage. L2 larvae are functionally analogous to C. elegans dauers, but their formation may be initiated by developmental rather than environmental cues. Because the molecular machinery controlling this process is most likely conserved, our goal is to identify and characterize homologs of dauer pathway genes in plant-parasitic nematodes. Knowledge gained will be used to develop novel, specific control strategies for these pests. A second area of research concerns plant-parasitic nematode sex determination, particularly in parthenogenetic species (eg., root-knot). Because female plant-parasitic nematodes are primarily responsible for crop damage, any control strategy which would interfere with female development would be advantageous. Sex determination in the root-knot nematode is strongly influenced by environmental cues. However, it is likely that the genes controlling the male/female decision are similar to those identified in C. elegans. We have constructed transgenic tobacco cell lines and plants which carry secreted or cytosolic versions of the C. elegans masculinizing hormone her-1 cDNA, driven by a constitutive (CaMV35S) or feeding-site-specific (TobRB7) promoters. These lines are being tested for the expression of functional her-1 protein and for the ability to perturb normal sex determination of infecting root-knot nematodes.

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