40 research outputs found
Genome-wide analyses of Liberibacter species provides insights into evolution, phylogenetic relationships, and virulence factors.
'Candidatus Liberibacter' species are insect-transmitted, phloem-limited α-Proteobacteria in the order of Rhizobiales. The citrus industry is facing significant challenges due to huanglongbing, associated with infection from 'Candidatus Liberibacter asiaticus' (Las). In order to gain greater insight into 'Ca. Liberibacter' biology and genetic diversity, we have performed genome sequencing and comparative analyses of diverse 'Ca. Liberibacter' species, including those that can infect citrus. Our phylogenetic analysis differentiates 'Ca. Liberibacter' species and Rhizobiales in separate clades and suggests stepwise evolution from a common ancestor splitting first into nonpathogenic Liberibacter crescens followed by diversification of pathogenic 'Ca. Liberibacter' species. Further analysis of Las genomes from different geographical locations revealed diversity among isolates from the United States. Our phylogenetic study also indicates multiple Las introduction events in California and spread of the pathogen from Florida to Texas. Texan Las isolates were closely related, while Florida and Asian isolates exhibited the most genetic variation. We have identified conserved Sec translocon (SEC)-dependent effectors likely involved in bacterial survival and virulence of Las and analysed their expression in their plant host (citrus) and insect vector (Diaphorina citri). Individual SEC-dependent effectors exhibited differential expression patterns between host and vector, indicating that Las uses its effector repertoire to differentially modulate diverse organisms. Collectively, this work provides insights into the evolution of 'Ca. Liberibacter' species, the introduction of Las in the United States and identifies promising Las targets for disease management
Motor-Driven Bacterial Flagella and Buckling Instabilities
Many types of bacteria swim by rotating a bundle of helical filaments also
called flagella. Each filament is driven by a rotary motor and a very flexible
hook transmits the motor torque to the filament. We model it by discretizing
Kirchhoff's elastic-rod theory and develop a coarse-grained approach for
driving the helical filament by a motor torque. A rotating flagellum generates
a thrust force, which pushes the cell body forward and which increases with the
motor torque. We fix the rotating flagellum in space and show that it buckles
under the thrust force at a critical motor torque. Buckling becomes visible as
a supercritical Hopf bifurcation in the thrust force. A second buckling
transition occurs at an even higher motor torque. We attach the flagellum to a
spherical cell body and also observe the first buckling transition during
locomotion. By changing the size of the cell body, we vary the necessary thrust
force and thereby obtain a characteristic relation between the critical thrust
force and motor torque. We present a sophisticated analytical model for the
buckling transition based on a helical rod which quantitatively reproduces the
critical force-torque relation. Real values for motor torque, cell body size,
and the geometry of the helical filament suggest that buckling should occur in
single bacterial flagella. We also find that the orientation of pulling
flagella along the driving torque is not stable and comment on the biological
relevance for marine bacteria.Comment: 15 pages, 11 figure
Chaperone‐mediated coupling of subunit availability to activation of flagellar Type III secretion
Bacterial flagellar subunits are exported across the cell membrane by the flagellar Type III Secretion System (fT3SS), powered by the proton motive force (pmf) and a specialized ATPase that enables the flagellar export gate to utilize the pmf electric potential (ΔΨ). Export gate activation is mediated by the ATPase stalk, FliJ, but how this process is regulated to prevent wasteful dissipation of pmf in the absence of subunit cargo is not known. Here, we show that FliJ activation of the export gate is regulated by flagellar export chaperones. FliJ binds unladen chaperones and, by using novel chaperone variants specifically defective for FliJ binding, we show that disruption of this interaction attenuates motility and cognate subunit export. We demonstrate in vitro that chaperones and the FlhA export gate component compete for binding to FliJ, and show in vivo that unladen chaperones, which would be present in the cell when subunit levels are low, sequester FliJ to prevent activation of the export gate and attenuate subunit export. Our data indicate a mechanism whereby chaperones couple availability of subunit cargo to pmf-driven export by the fT3SS