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      Fusarium Wilt of Banana: Current Knowledge on Epidemiology and Research Needs Toward Sustainable Disease Management

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          Abstract

          Banana production is seriously threatened by Fusarium wilt (FW), a disease caused by the soil-borne fungus Fusarium oxysporum f. sp. cubense ( Foc). In the mid-twentieth century FW, also known as “Panama disease”, wiped out the Gros Michel banana industry in Central America. The devastation caused by Foc race 1 was mitigated by a shift to resistant Cavendish cultivars, which are currently the source of 99% of banana exports. However, a new strain of Foc, the tropical race 4 (TR4), attacks Cavendish clones and a diverse range of other banana varieties. Foc TR4 has been restricted to East and parts of Southeast Asia for more than 20 years, but since 2010 the disease has spread westward into five additional countries in Southeast and South Asia (Vietnam, Laos, Myanmar, India, and Pakistan) and at the transcontinental level into the Middle East (Oman, Jordan, Lebanon, and Israel) and Africa (Mozambique). The spread of Foc TR4 is of great concern due to the limited knowledge about key aspects of disease epidemiology and the lack of effective management models, including resistant varieties and soil management approaches. In this review we summarize the current knowledge on the epidemiology of FW of banana, highlighting knowledge gaps in pathogen survival and dispersal, factors driving disease intensity, soil and plant microbiome and the dynamics of the disease. Comparisons with FW in other crops were also made to indicate possible differences and commonalities. Our current understanding of the role of main biotic and abiotic factors on disease intensity is reviewed, highlighting research needs and futures directions. Finally, a set of practices and their impact on disease intensity are discussed and proposed as an integrative management approach that could eventually be used by a range of users, including plant protection organizations, researchers, extension workers and growers.

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          Most cited references135

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          Pathogen population genetics, evolutionary potential, and durable resistance.

          We hypothesize that the evolutionary potential of a pathogen population is reflected in its population genetic structure. Pathogen populations with a high evolutionary potential are more likely to overcome genetic resistance than pathogen populations with a low evolutionary potential. We propose a flexible framework to predict the evolutionary potential of pathogen populations based on analysis of their genetic structure. According to this framework, pathogens that pose the greatest risk of breaking down resistance genes have a mixed reproduction system, a high potential for genotype flow, large effective population sizes, and high mutation rates. The lowest risk pathogens are those with strict asexual reproduction, low potential for gene flow, small effective population sizes, and low mutation rates. We present examples of high-risk and low-risk pathogens. We propose general guidelines for a rational approach to breed durable resistance according to the evolutionary potential of the pathogen.
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            The Plant Cell Wall: A Dynamic Barrier Against Pathogen Invasion

            Prospective plant pathogens must overcome the physical barrier presented by the plant cell wall. In addition to being a preformed, passive barrier limiting access of pathogens to plant cells, the cell wall is actively remodeled and reinforced specifically at discrete sites of interaction with potentially pathogenic microbes. Active reinforcement of the cell wall through the deposition of cell wall appositions, referred to as papillae, is an early response to perception of numerous categories of pathogens including fungi and bacteria. Rapid deposition of papillae is generally correlated with resistance to fungal pathogens that attempt to penetrate plant cell walls for the establishment of feeding structures. Despite the ubiquity and apparent importance of this early defense response, relatively little is known about the underlying molecular mechanisms and cellular processes involved in the targeting and assembly of papillae. This review summarizes recent advances in our understanding of cell wall-associated defenses induced by pathogen perception as well as the impact of changes in cell wall polymers on interactions with pathogens and highlights significant unanswered questions driving future research in the area.
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              A small, cysteine-rich protein secreted by Fusarium oxysporum during colonization of xylem vessels is required for I-3-mediated resistance in tomato.

              A 12 kDa cysteine-rich protein is secreted by Fusarium oxysporum f. sp. lycopersici during colonization of tomato xylem vessels. Peptide sequences obtained with mass spectrometry allowed identification of the coding sequence. The gene encodes a 32 kDa protein, designated Six1 for secreted in xylem 1. The central part of Six1 corresponds to the 12 kDa protein found in xylem sap of infected plants. A mutant that had gained virulence on a tomato line with the I-3 resistance gene was found to have lost the SIX1 gene along with neighbouring sequences. Transformation of this mutant with SIX1 restored avirulence on the I-3 line. Conversely, deletion of the SIX1 gene in a wild-type strain results in breaking of I-3-mediated resistance. These results suggest that I-3-mediated resistance is based on recognition of Six1 secreted in xylem vessels. Copyright 2004 Blackwell Publishing Ltd
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                Author and article information

                Contributors
                Journal
                Front Plant Sci
                Front Plant Sci
                Front. Plant Sci.
                Frontiers in Plant Science
                Frontiers Media S.A.
                1664-462X
                19 October 2018
                2018
                : 9
                : 1468
                Affiliations
                [1] 1Embrapa Mandioca e Fruticultura , Bahia, Brazil
                [2] 2Bioversity International , Montpellier, France
                [3] 3Institute of Environment, Natural Resources and Biodiversity, Universidad de León , León, Spain
                [4] 4Departamento de Fitopatologia, Universidade Federal de Viçosa , Viçosa, Brazil
                Author notes

                Edited by: Dirk Albert Balmer, Syngenta, Switzerland

                Reviewed by: Noelani Van Den Berg, University of Pretoria, South Africa; Andrés A. Borges, Consejo Superior de Investigaciones Científicas (CSIC), Spain

                *Correspondence: Miguel Dita miguel.dita@ 123456embrapa.br

                This article was submitted to Plant Microbe Interactions, a section of the journal Frontiers in Plant Science

                Article
                10.3389/fpls.2018.01468
                6202804
                30405651
                6144e32f-1c30-439e-8edb-9cad89cfcd10
                Copyright © 2018 Dita, Barquero, Heck, Mizubuti and Staver.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 06 June 2018
                : 18 September 2018
                Page count
                Figures: 4, Tables: 1, Equations: 0, References: 162, Pages: 21, Words: 18634
                Funding
                Funded by: Fundação Instituto de Pesquisas Econômicas 10.13039/501100001807
                Award ID: 2015/03625-7
                Categories
                Plant Science
                Review

                Plant science & Botany
                musa spp,panama disease,fusarium oxysporum f. sp. cubense,integrated pest management,epidemiology

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