EC Number   |
General Information |
Reference |
|---|
  2.7.8.31 | malfunction |
a gumD mutant, isolated from Xc17 by gene replacement possesses altered pigment xanthomonadin profiles and exhibits reduced virulence in causing black rot in broccoli |
702006 |
| 2.7.8.31 | malfunction |
extracellular polysaccharide-defective mutants of Xanthomonas axonopodis pv. manihotis are created by targeted disruption of the gumD gene |
713218 |
| 2.7.8.31 | malfunction |
from the biochemical analysis of a defined set of Xanthomonas campestris gum mutants, experimental data are reported for assigning functions to the products of the gum genes. Inactivation of gumD completely abolishes in vitro polymer formation. The gumD- mutant is the unique mutant strain, generated in a wild-type background, that shows no released labeled oligosaccharides when permeabilized cells are labeled with UDP-[14C]glucose. Cells labeled with UDP-[14C]glucuronic acid or GDP-[14C]mannose show similar results. The C-terminal portion of GumD is cloned into broad-host-range vector pRK404, producing plasmid pCD2. This plasmid complements the xanthan defect in the XcD strain, rendering mucoid colonies |
704257 |
| 2.7.8.31 | malfunction |
significantly attenuated production of xanthan in knock-out mutant strain SJ1017 |
702828 |
| 2.7.8.31 | malfunction |
the gumD deletion mutant exhibits reduced biofilm and extracellular polysaccharides production and attenuated virulence on rice |
723608 |
| 2.7.8.31 | malfunction |
the gumD deletion mutant is negative in xanthan production, grows well, but its colonies are smaller and non-mucoid |
-, 722853 |
| 2.7.8.31 | malfunction |
xanthan-deficient mutants of Xanthomonas axonopodis pv. citri, the bacterium responsible for citrus canker, are generated by deletion and marker exchange of the region encoding the carboxy-terminal end of the first glycosyltransferase, GumD. Mutants of gumD do not produce xanthan and remain pathogenic in citrus plants to the same extent as wild-type bacteria. The kinetics of appearance of initial symptoms, areas of plant material affected, and growth of bacteria inside plant tissue throughout the disease process are similar for both wild-type and mutant inoculations. Exopolysaccharide deffciency does not impair the ability of the bacteria to induce hypersensitive response on non-host plants. Apart from variations in phenotypic aspects, no differences in growth or survival under diVerent stress conditions are observed between the xanthan-deficient mutant and wild-type bacteria. gumD mutants display impaired survival under oxidative stress during stationary phase as well as impaired epiphytic survival on citrus leaves |
701945 |
| 2.7.8.31 | metabolism |
the GumD protein catalyses the first step of xanthan production and is responsible for the addition of the first glucose molecule to the isoprenoid acceptor molecule |
713218 |
| 2.7.8.31 | physiological function |
gumD-dependent extracellular polysaccharides contribute to biofilm formation |
723608 |
| 2.7.8.31 | physiological function |
GumH is involved in biosynthesis of the pentasaccharide repeating unit of xanthan |
702828 |
