Pathogen free plants slideshare

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Host pathogen interaction plants. Upcoming SlideShare. Like this presentation? Why not share!

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Plant Cell wall and its role in def Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode.

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Sheikh MansoorResearch Associate Follow. Published in: Education. Full Name Comment goes here.Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. If you continue browsing the site, you agree to the use of cookies on this website. See our User Agreement and Privacy Policy. See our Privacy Policy and User Agreement for details. Published on Oct 8, SlideShare Explore Search You. Submit Search. Home Explore. Successfully reported this slideshow.

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We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime. Introduction to Virus Free Plant tissue Culture. Upcoming SlideShare. Like this presentation? Why not share! Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode. Praveen kumar verma Follow. Published in: Science. Full Name Comment goes here. Are you sure you want to Yes No. Srijan Verma. Jyotirmayee Barik. Show More. No Downloads.

Views Total views. Actions Shares. No notes for slide. Introduction to Virus Free Plant tissue Culture 1. Inthey recovered virus free potato. This attained wide application of plant tissue culture to raise virus free plants in agriculture. Flow diagram of Meristem culture 8. Thank you. You just clipped your first slide! Clipping is a handy way to collect important slides you want to go back to later.

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pathogen free plants slideshare

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See our Privacy Policy and User Agreement for details. Published on Jan 12, This presentation is on plant pathogen interaction. SlideShare Explore Search You. Submit Search.

pathogen free plants slideshare

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pathogen free plants slideshare

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No Downloads. Views Total views. Actions Shares. No notes for slide. Plant Pathogen Interaction 1.Plant disease resistance protects plants from pathogens in two ways: by pre-formed structures and chemicals, and by infection-induced responses of the immune system. Disease outcome is determined by the three-way interaction of the pathogen, the plant and the environmental conditions an interaction known as the disease triangle.

Defense-activating compounds can move cell-to-cell and systematically through the plant's vascular system. However, plants do not have circulating immune cellsso most cell types exhibit a broad suite of antimicrobial defenses.

Plants consistently resist certain pathogens but succumb to others; resistance is usually specific to certain pathogen species or pathogen strains. Plant disease resistance is crucial to the reliable production of food, and it provides significant reductions in agricultural use of land, water, fuel and other inputs.

Plants in both natural and cultivated populations carry inherent disease resistance, but this has not always protected them. The late blight Great Famine of Ireland of the s was caused by the oomycete Phytophthora infestans.

The current wheat stem rustleaf rust and yellow stripe rust epidemics spreading from East Africa into the Indian subcontinent are caused by rust fungi Puccinia graminis and P. Other epidemics include Chestnut blightas well as recurrent severe plant diseases such as Rice blastSoybean cyst nematodeCitrus canker.

Plant pathogens can spread rapidly over great distances, vectored by water, wind, insects, and humans. However, disease control is reasonably successful for most crops. Disease control is achieved by use of plants that have been bred for good resistance to many diseases, and by plant cultivation approaches such as crop rotationpathogen-free seed, appropriate planting date and plant density, control of field moisture, and pesticide use.

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The plant immune system carries two interconnected tiers of receptors, one most frequently sensing molecules outside the cell and the other most frequently sensing molecules inside the cell. Both systems sense the intruder and respond by activating antimicrobial defenses in the infected cell and neighboring cells. In some cases, defense-activating signals spread to the rest of the plant or even to neighboring plants.

The two systems detect different types of pathogen molecules and classes of plant receptor proteins. The first tier is primarily governed by pattern recognition receptors that are activated by recognition of evolutionarily conserved pathogen or microbial—associated molecular patterns PAMPs or MAMPs.

Activation of PRRs leads to intracellular signaling, transcriptional reprogramming, and biosynthesis of a complex output response that limits colonization.

The second tier, primarily governed by R gene products, is often termed effector-triggered immunity ETI. ETI is typically activated by the presence of specific pathogen "effectors" and then triggers strong antimicrobial responses see R gene section below. In addition to PTI and ETI, plant defenses can be activated by the sensing of damage-associated compounds DAMPsuch as portions of the plant cell wall released during pathogenic infection.

Responses activated by PTI and ETI receptors include ion channel gating, oxidative burstcellular redox changes, or protein kinase cascades that directly activate cellular changes such as cell wall reinforcement or antimicrobial productionor activate changes in gene expression that then elevate other defensive responses.

Plant immune systems show some mechanistic similarities with the immune systems of insects and mammals, but also exhibit many plant-specific characteristics. The defenses induced by MAMP perception are sufficient to repel most pathogens. However, pathogen effector proteins see below are adapted to suppress basal defenses such as PTI.

The ETI response is reliant on R genesand is activated by specific pathogen strains. Plant ETI often causes an apoptotic hypersensitive response. Plants have evolved R genes resistance genes whose products mediate resistance to specific virus, bacteria, oomycete, fungus, nematode or insect strains. R gene products are proteins that allow recognition of specific pathogen effectors, either through direct binding or by recognition of the effector's alteration of a host protein.

Most plant immune systems carry a repertoire of different R gene homologs. Individual R genes have been demonstrated to mediate resistance to specific virus, bacteria, oomycete, fungus, nematode or insect strains. Studied R genes usually confer specificity for particular strains of a pathogen species those that express the recognized effector.

As first noted by Harold Flor in his midth century formulation of the gene-for-gene relationshipa plant R gene has specificity for a pathogen avirulence gene Avr gene. Avirulence genes are now known to encode effectors.

Effectors are central to the pathogenic or symbiotic potential of microbes and microscopic plant-colonizing animals such as nematodes. These colonist-derived effectors manipulate the host's cell physiology and development. As such, effectors offer examples of co-evolution example: a fungal protein that functions outside of the fungus but inside of plant cells has evolved to take on plant-specific functions.Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising.

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Plant disease resistance

See our Privacy Policy and User Agreement for details. Published on Jan 1, A detailed project on plant diseases,causes, symptoms and control measures with illustrations.

The project explains in brief fungal and bacterial and and their control measures. Blast disease, citrus canker and leaf mosaic disease of tapioca are explained in detail. Non - infectious diseases are also mentioned. SlideShare Explore Search You. Submit Search.

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Upcoming SlideShare. Like this presentation? Why not share! Introduction to Greenhouse Diseases Embed Size px.Our final choice is the easy on the eye Oosty after an encouraging season to date. The conditions should not trouble the 2010 Open Champion who is a brilliant links player, always strikes the ball purely and is a decent scrambler.

He looks a bit of value at 67. What can we expect from Erin Hills. Strikers have been the talk of the town so far this season, with Romelu Lukaku, Harry Kane and Alvaro Morata among those blazing a trail.

There were glimpses of Palace being more organised against City but in the end they still got stuffed. Roy will be looking to get this trio of games out the way before his work in keeping Palace safe can begin in earnest. With City scoring goals left, right and centre United know they need another big win to keep pace. To be honest, no one inside the game was overly worried about that sort of stuff but it was in the media a lot and has now been put to bed.

Morata is the new guy on the block but he has hit the ground running, while Aguero has being doing it for years now in the Premier League. Chelsea did the double over City last year and from my experience when that happens you are even more fired up to go back and do well. The Brighton result will have brought Newcastle back down to earth after they picked up a head of steam.

The boffins at Sun Bets tell me there has never been a Premier League game end 0-0 between these sides too so expect goals. By continuing to use the site, you agree to the use of cookies. You can change this and find out more by following this link'The Sun', 'Sun', 'Sun Online' and 'Dream Team' are registered trademarks or trade names of News Group Newspapers Limited. This service is provided by News Group Newspapers. Both companies registered in England with registered offices located at 1 London Bridge Street, London, SE1 9GF.

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