Sphingolipid homeostasis: How do cells know when enough is enough? Implications for plant pathogen responses.

Sphingolipid homeostatic regulation is important for balancing plant life and death. Plant cells finely tune sphingolipid biosynthesis to ensure sufficient levels to support growth through their basal functions as major components of endomembranes and the plasma membrane. Conversely, accumulation of sphingolipid biosynthetic intermediates, long-chain bases (LCBs) and ceramides, is associated with programmed cell death.

Characterization of Soybean Events with Enhanced Expression of the Microtubule-Associated Protein 65-1 (MAP65-1).

Microtubule-associated protein 65-1 (MAP65-1) protein plays an essential role in plant cellular dynamics through impacting stabilization of the cytoskeleton by serving as a crosslinker of microtubules. The role of MAP65-1 in plants has been associated with phenotypic outcomes in response to various environmental stresses. The MAP65-1 (MAP65-1) is a known virulence target of plant bacterial pathogens and is thus a component of plant immunity.

A phytobacterial TIR domain effector manipulates NAD to promote virulence.

The Pseudomonas syringae DC3000 type III effector HopAM1 suppresses plant immunity and contains a Toll/interleukin-1 receptor (TIR) domain homologous to immunity-related TIR domains of plant nucleotide-binding leucine-rich repeat receptors that hydrolyze nicotinamide adenine dinucleotide (NAD ) and activate immunity. In vitro and in vivo assays were conducted to determine if HopAM1 hydrolyzes NAD and if the activity is essential for HopAM1's suppression of plant immunity and contribution to virulence. HPLC and LC-MS were utilized to analyze metabolites produced from NAD by HopAM1 in vitro and in both yeast and plants.

Pathogenic Bacteria Target Plant Plasmodesmata to Colonize and Invade Surrounding Tissues.

A hallmark of multicellular organisms is their ability to maintain physiological homeostasis by communicating among cells, tissues, and organs. In plants, intercellular communication is largely dependent on plasmodesmata (PD), which are membrane-lined channels connecting adjacent plant cells. Upon immune stimulation, plants close PD as part of their immune responses.

Activation-Dependent Destruction of a Co-receptor by a Pseudomonas syringae Effector Dampens Plant Immunity.

The Arabidopsis immune receptor FLS2 and co-receptor BAK1 perceive the bacterial flagellin epitope flg22 to activate plant immunity. To prevent this response, phytopathogenic bacteria deploy a repertoire of effector proteins to perturb immune signaling. However, the effector-induced perturbation is often sensed by the host, triggering another layer of immunity.

A Bacterial Effector Co-opts Calmodulin to Target the Plant Microtubule Network.

The bacterial pathogen Pseudomonas syringae depends on effector proteins secreted by its type III secretion system for the pathogenesis of plants. The majority of these effector proteins are known suppressors of immunity, but their plant targets remain elusive. Using Arabidopsis thaliana as a model host, we report that the HopE1 effector uses the host calcium sensor, calmodulin (CaM), as a co-factor to target the microtubule-associated protein 65 (MAP65), an important component of the microtubule network.