Plant-Pathogen Interactions - Science topic

I am planning to study adaptation strategies of farmers to climate

What could be the probable techniques applied from transcriptomics to study metabolomics of plant pathogen interaction ?

Need suggestion.

Hello everybody,

I work on plant science, more specificlly in plant pathogen interaction. In my project I need to analyse an interaction of some proteins related to host and virus interaction, but before I'd like to do this analyses in silico.

Do you have any idea of a good software/program, online or not?

Reactive oxygen species are produced during early plant-pathogen interactions as a plant defence response. Sometimes, necrotrophic pathogens also produce ROS to cause necrosis or plant cell death. Now the question arises, how can we distinguish between both the ROS, specially during infection? Is there any approach available to do so?

How can we determine which pathogen (bacteria, fungi, virus) is responsible for a given plant disease from a phenotypic observation (for example: spots, smudges on leaves) ??

What are the potential effects of on interactions between nonvectors and vectors on the spread of plant pathogens in managed and natural ecosystems?

Previous studies have shown that different herbivore and plant pathogen species elicit different hormone responses in plants.

Mediated by plant defenses, could herbivores and plant pathogens interact to affect the spread of the disease across landscapes?

Any thoughts?

Dear all,

We are going to use the Maxi-Pam (Imaging) to measure chlorophyll fluorescence and measure classic parameters in Arabidopsis leave or in potted plants (plant-pathogens interaction), and I'm looking for a reliable method to use this system in routine or some help to start. There are so many possibilities...And also, does anyone use green light in work room when you need to transfer your dark adapted plants? Do you wear some protection from blue light like glasses, when you don't use the red perspex hood? Many thanks, Alina

I want to perform genome wide association mapping for plant disease resistance gene. Since, I am completely a beginner in this field, it would be really helpful if someone can give me some advice on how to approach, how to design the GWAS pipeline, valuable publications etc. The genotyping and phenotyping of my genotypes have been done. I have all the data.

Looking forward to your help.

does anyone know how to give biotic stress to rice, if i have a specific bacterial culyure and want to see the effect of rice under biotic stress so what procedure should i use?

I was analyzing several examples of plant pathogen interaction (pathosystems) and I was wondering if cell expansion comes first or second to cell division. Of course, I must considered that everything happens after a PAMP sequence of events and also to possible recognition of pathogen by plant cells.

Does anybody have some clues?

Thanks and Regards,

Dr. Joao Paulo R. Marques

Can any one guide me about what are all the insilico analysis I can do with defense genes I have isolated or obtained through Transcriptome sequencing of a resistant variety of black pepper after challenge inoculation with Phytophthora capsici

I have done expression analysis of these defense genes through qPCR. There are about 40 number of defense genes or defense related genes. I have very little knowledge about insilico tools and bioinformatics techniques.Kindly help

I want to know wich are the better tissues that i can use, if depend of the local that  the pathogen attack or the tissue content. Etc.

Can any one guide me about what are all the insilico analysis I can do with defense genes I have isolated or obtained through Transcriptome sequencing of a resistant variety of black pepper after challenge inoculation with Phytophthora capsici I have done expression analysis of these defense genes through qPCR. There are about 40 number of defense genes or defense related genes. I have very little knowledge about insilico tools and bioinformatics techniques.Kindly help

Hello.

Nowadays, I am studying on seed storage protein in wheat and their relatives.

HMW glutenin is well-known and it has been studied a lot, but LMW glutenin has studied less than HMW glutenin although LMW has a relatively shorter sequence than HMW because it is harder to distinguish LMW bands than HMW bands.

Glu-1 encodes HMW glutenins, and a lot of Glu-1 such as Glu-A1, Glu-B1, Glu-D1 in wheat, Glu-H1 in barley, and Glu-R1 in rye have been characterized.

However, I couldn't find Glu-R3 in Secale cereale. I could find only one study about Glu-R3 in Secale sylvestre. But as far as I know, Secale sylvestre is not a cultivated rye but a kind of wild rye. Also, there is no Glu-R3 protein or nucleotide information of S. cereale in NCBI database. 

I want to know LMW glutenin in Secale cereale because it can affect to the quality of 1RS wheat-rye translocation varieties. I can't find any related reference. Please help me.

Intuitively, this kind of infection would be detrimental to the host because there are more things exploiting it. But assuming that there is interference competition between the two species, isn’t it possible for them to lower each other’s pathogenicity because of the mutual reduction in fitness?

Broadly, SA induces defense against biotrophic pathogens, whereas JA activates defense against necrotrophic pathogens. Are there any reports regarding the synergistic relation of salicylic and jasmonic acids in pathogen defense, especially against necrotrophs?

Many thanks in advance.

Plant probiotic bacteria are known to enhance salinity tolerance in host plant. However, mechanism of their action on host plants are poorly understood. We wish to study the underlying molecular mechanisms plant probiotic bacteria in enhancing salinity tolerance in rice.

I am investigating the defense mechanism of an edible crop to Xanthomonas infection. I would like to know how to determine the sample collection and analysis time points e.g. 2, 4, 8, 24, 48, hours post inoculation (hpi) and what is the duration of the experiment e.g. 5 days post-inoculation? Can these same time points be used when analyzing for metabolomic studies?

My work is on the assessment of the SAR ( Systemic acquired Resistance) and ISR (Induced Systemic Resistance) by the measurement of some molecular markers such as Phytohormones and proteines.

I am interested to learn about other elicitors than chitosan which can be used to induce responses like upon pathogen infection in the moss Physcomitrella patens. Thanks a lot for your suggestions!

Plant apoplast contains various antimicrobial peptides e.g., defensins. As part of their antifungal mode of action, these defensins (not all defensins) are known to interact specifically with membrane-resident bioactive phospholipids, such as PA, PI(4,5)P2 with high affinity.  We know that these pathogens have different life style. Very importantly, when biotrophic pathogens thrive in the apoplst, they encounter various antifungal proteins and fungus needs to protect itself from these proteins which subsequently determine the outcome.  However, necrotrophic pathogens produce different cell wall-degrading enzymes (CWDEs) and toxins to kill the host plant cell.  When necrotrophic pathogens damage the cell wall and plasma membrane, the antimicrobial peptides (e.g., defensins) which are present in the apoplast, may encounter plant membrane-resident bioactive phospholipids. Do you think these defensins highly interact with plant phospholipids (instead of fungal membrane-resident bioactive phospholipids) and indirectly regulate its own plant lipid metabolism? If so, why does it prefer binding to its own phospholipids? Does this non-specific interaction leads to toxicity to the plant cells? What about binding to fungal membrane-resident bioactive phospholipids? Does defensin loses it ability to bind to fungal phospholipids, subsequently paving the way to infect the plant? How do transgenic (and also non-transgenic) plants over expressing phospholipid-binding proteins (e.g., defensins) control itself of these non-specific interactions?  Do you think the change in the environment (e.g., pH) can limit these non-specific interactions in both non-transgenic and overexpressing plants ?

Hi All, 

Please here are some other pictures that I got. May somebody help me with the name of this fungus? I am working on water hyacinth and these pictures come from damage leaves by pathogens

Thanks

As I have found, endophytic fungi mostly belong to the phylum Ascomycota and Basidiomycota.Has there been any other report of endophytic fungi belonging to phylum other than these two?

Any one can discuss or suggest the role of reactive oxygen species and its production during such type of interaction.

.i am researcher student of M.phil.My field is Environmental microbiology.where i want to know that how digestate effects on plant growth and inhibiting effect on plant pathogen (fungus) in soil (drought condition)

As we know that the Macrophomina is the pycnidial stage, so where exactly the pycnidial stage form naturally.

I will start a work on plant-pathogen interaction and I want to know if biotrophic fungi can secret elicitors in order to modify the transcription factors in the host. I am reading some papers related to inactivation of MAPKs fo suppress PTI (Zhang et al., 2007 Cell Host and Microbe 1: 175-185) but I really want to learn if fungal elicitors can interfere in MYB or WRKY transcriptor factors. Can anyone help me with this topic?

As we know that charcoal rot appear during stress period. Afterall pest and disease creates stress to plant.

Is there any relation between them?

Any ongoing research work on the use of mycoviruses in India for the biocontrol of plant pathogens?

Do essential oils cause leaf scorching on leaves of the plants? Or do they have certain mechanisms of somehow "burning" or causing scorch when applied on the leaves? Thank you!!! 

In plant-pathogen interactions, horizontal/ lateral gene transfers are well known to challenge each other. But, these are results of 'transfer of biosynthetic machineries' (operons, gene clusters, repetitive elements etc.) as a result of 'physical transfer' during the course of evolution. But, does this interaction between  plant and it's pathogens leave 'signatures' (patterns that mimic a defense response, circadian patterns, adaptive mutations in genes, suppressions, leading to super-active promoters etc.) in genes, proteins, inter-genic regions in the forms of signatures that is tracable using molecular techniques or computational efforts ? If yes, then how to trace these signatures and assign them to specific interactions (beneficial vs. harmful bacteria/ fungi/ nematodes )?

Plant nematology

I want to determine the resting spore population present in Barley roots. if anybody can suggest how a single resting spore of Polymyxa graminis looks like, while resting spore suspension prepared by crushing the roots.

I have many isolates of Pyrenophora teres and i want to know the fsp for them, is ITS region sequencing give me a good results for that.

Damaged were beech seedlings planted in the spring 2015. The bark and phloem were damaged mainly shallow, on the several places were feeding spots oval and deeper. The feeding (probably insects) was mainly in the root neck area, but so in higher part of the seedlings, approximately in 20-30 (40) cm above ground. We found in the old German books (Escherich, Altum, Nüsslin), that similar damage was created from European hornet (Vespa crabro).

Is there a way to analyse any possible inhibition effects of one pathogen on the other or possibly any other interactions between them ? e.g. one pathogen might just weaken the plant defenses without causing any symptoms, therefore facilitating easiest infection of the symptom-causing pathogen...

will it be easier to do with RACE?

Nail polish can't be peeled off and the epidermal tissue doesn't come off that easily.

I need sequence information of above genes in Nicotiana benthamiana but I could not find. Every time I look for nicotiana benthamiana NCBI giving info about Nicotiana tabacum. liitle confused.. please help

The main goals are to maintain vigor and pathogenicity of the isolates, avoiding contamination.

Thanks.

I would like to simulate a fungal infection of Altenaria sp. because unfortunatelly we can not grow plants with the fungus. Any ellicitor to do? What do you think about mechanical injury?

Thank you in advance

Raquel

I am having problems observing the inhibition effects of Leonurus sibiricus and L. japonicus extracts against crop pathogenic fungi by using the disk diffusion method.

Therefore, I plan to diffuse the extracts directly into the PDA, and then inoculate the fungi samples into the media. However, I am confused by the ratio between the volume of extracts and PDA that will be mixed together. Any suggestions?

e.g. high concentrations of SA or interaction with abiotic stress factors and promoting its negative effect? Many authors indicate that SA has a beneficial role in plant-pathogen interactions or exogenous application alleviate the negative effect of salt stress. I'm interested in different roles of SA, what happened with plants when overproduction of SA has taken place (except conversion to less toxic form)? Maybe you know some publications, I have problems with finding. I know that SA can cause oxidative stress, but maybe you can help me more in this area.

Does anyone know whether sulfur, iron, or copper may play a role in corn plant chemical defenses?  Jasmonic acid, DIMBOA, or production of any other chemical compound?  I know that sulfur is important for glucosinolate production, but to my knowledge corn doesn't employ glucosinolates.  Any references would be much appreciated.  Thanks!

Suppose I want want to design ANN and SVM model for designing siRNA against plant pathogen. Is it possible to take Hueskan (2431) dataset for testing and training purposes because Huesken dataset is mammalian? Also, I want to know whether there is any standard siRNA plant dataset with respective efficacy. 

Hello,

I need to infect my plants with powdery mildew to check if they become more susceptible to the infection. Currently in my lab, we just drop spores and try to do it as evenly as possible. But I think it should be a more accurate method to infect plants. Do you know any protocols? Also, how do you check the results of the infection? 

Which soybean seedborne Fusarium species can we expect to find in a soybean seed lot? Do we actually know that? Are seedborne Fusarium species plant pathogens?

How close related those species are? What about their pathogenicity to plants? 

Can anyone recommend where I can get (commercially for research purposes) nematodes (Meloidogyne spp) infecting Phaseolus vulgaris (bean) or any nematode infecting Helianthus annuus (sun flower)?

I want to test the genetic diversity between F. graminearum ? what is the best method and what is the best primers to use?

I have been consistently observing that corn seedling radicles are much more extensively damaged by pathogens, compared to the seminal roots of the same seedlings. Can anyone point me to some literature on why this might be the case?