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Xanthomonas albilineans needs an OmpA family outer protein for disease symptom development and multiplication in the sugarcane stalk
Xanthomonas albilineans (Xa) is a systemic, xylem-invading pathogen that causes sugarcane leaf scald. Xa produces albicidin, a potent antibiotic and phytotoxin which blocks chloroplast differentiation, thus causing the foliar symptoms of the disease. Albicidin is the only known pathogenicity factor...
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Published in: | Phytopathology 2010-06, Vol.100 (6), p.S110-S110 |
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description | Xanthomonas albilineans (Xa) is a systemic, xylem-invading pathogen that causes sugarcane leaf scald. Xa produces albicidin, a potent antibiotic and phytotoxin which blocks chloroplast differentiation, thus causing the foliar symptoms of the disease. Albicidin is the only known pathogenicity factor in Xa, yet albicidin deficient mutants are still able to colonize the sugarcane plant. In an attempt to identify other major pathogenicity factors, we screened 1,216 independent Tn5 insertions in Xa strain XaFL07-1 by single inoculation onto sugarcane cultivar CP80-1743. Mutants were screened for reduced pathogenicity (i.e., capacity to induce leaf symptoms and to multiply in the sugarcane stalk). Five independent Tn5 insertions were found in gene XALc_0557, which is predicted to encode an OmpA family outer membrane protein. Each of these insertions resulted in a mutant strain that elicited very slight to no symptoms and was not able to move as efficiently within the sugarcane stalk, both spatially and in intensity, as wild type XaFL07-1. Additional phenotypic studies showed that these mutants: 1) produced albicidin, 2) were less motile and 3) were slower growing than the wild type Xa in vitro. However, these OmpA mutants were able to multiply in sugarcane leaf tissue to levels similar to the wild-type strain XaFL07-1. Complementation analyses are currently underway. |
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Xa produces albicidin, a potent antibiotic and phytotoxin which blocks chloroplast differentiation, thus causing the foliar symptoms of the disease. Albicidin is the only known pathogenicity factor in Xa, yet albicidin deficient mutants are still able to colonize the sugarcane plant. In an attempt to identify other major pathogenicity factors, we screened 1,216 independent Tn5 insertions in Xa strain XaFL07-1 by single inoculation onto sugarcane cultivar CP80-1743. Mutants were screened for reduced pathogenicity (i.e., capacity to induce leaf symptoms and to multiply in the sugarcane stalk). Five independent Tn5 insertions were found in gene XALc_0557, which is predicted to encode an OmpA family outer membrane protein. Each of these insertions resulted in a mutant strain that elicited very slight to no symptoms and was not able to move as efficiently within the sugarcane stalk, both spatially and in intensity, as wild type XaFL07-1. Additional phenotypic studies showed that these mutants: 1) produced albicidin, 2) were less motile and 3) were slower growing than the wild type Xa in vitro. However, these OmpA mutants were able to multiply in sugarcane leaf tissue to levels similar to the wild-type strain XaFL07-1. 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Xa produces albicidin, a potent antibiotic and phytotoxin which blocks chloroplast differentiation, thus causing the foliar symptoms of the disease. Albicidin is the only known pathogenicity factor in Xa, yet albicidin deficient mutants are still able to colonize the sugarcane plant. In an attempt to identify other major pathogenicity factors, we screened 1,216 independent Tn5 insertions in Xa strain XaFL07-1 by single inoculation onto sugarcane cultivar CP80-1743. Mutants were screened for reduced pathogenicity (i.e., capacity to induce leaf symptoms and to multiply in the sugarcane stalk). Five independent Tn5 insertions were found in gene XALc_0557, which is predicted to encode an OmpA family outer membrane protein. Each of these insertions resulted in a mutant strain that elicited very slight to no symptoms and was not able to move as efficiently within the sugarcane stalk, both spatially and in intensity, as wild type XaFL07-1. Additional phenotypic studies showed that these mutants: 1) produced albicidin, 2) were less motile and 3) were slower growing than the wild type Xa in vitro. However, these OmpA mutants were able to multiply in sugarcane leaf tissue to levels similar to the wild-type strain XaFL07-1. 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Xa produces albicidin, a potent antibiotic and phytotoxin which blocks chloroplast differentiation, thus causing the foliar symptoms of the disease. Albicidin is the only known pathogenicity factor in Xa, yet albicidin deficient mutants are still able to colonize the sugarcane plant. In an attempt to identify other major pathogenicity factors, we screened 1,216 independent Tn5 insertions in Xa strain XaFL07-1 by single inoculation onto sugarcane cultivar CP80-1743. Mutants were screened for reduced pathogenicity (i.e., capacity to induce leaf symptoms and to multiply in the sugarcane stalk). Five independent Tn5 insertions were found in gene XALc_0557, which is predicted to encode an OmpA family outer membrane protein. Each of these insertions resulted in a mutant strain that elicited very slight to no symptoms and was not able to move as efficiently within the sugarcane stalk, both spatially and in intensity, as wild type XaFL07-1. Additional phenotypic studies showed that these mutants: 1) produced albicidin, 2) were less motile and 3) were slower growing than the wild type Xa in vitro. However, these OmpA mutants were able to multiply in sugarcane leaf tissue to levels similar to the wild-type strain XaFL07-1. Complementation analyses are currently underway.</abstract></addata></record> |
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subjects | Xanthomonas albilineans |
title | Xanthomonas albilineans needs an OmpA family outer protein for disease symptom development and multiplication in the sugarcane stalk |
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