Built Shallow to Maintain Homeostasis and Persistent Infection: Insight into the Transcriptional Regulatory Network of the Gastric Human Pathogen Helicobacter pylori

Transcriptional regulatory networks (TRNs) transduce environmental signals into coordinated output expression of the genome. Accordingly, they are central for the adaptation of bacteria to their living environments and in host–pathogen interactions. Few attempts have been made to describe a TRN for a human pathogen, because even in model organisms, such as Escherichia coli, the analysis is hindered by the large number of transcription factors involved. In light of the paucity of regulators, the gastric human pathogen Helicobacter pylori represents a very appealing system for understanding how bacterial TRNs are wired up to support infection in the host. Herein, we review and analyze the available molecular and “-omic” data in a coherent ensemble, including protein–DNA and protein–protein interactions relevant for transcriptional control of pathogenic responses. The analysis covers ∼80% of the annotated H. pylori regulators, and provides to our knowledge the first in-depth description of a TRN for an important pathogen. The emerging picture indicates a shallow TRN, made of four main modules (origons) that process the physiological responses needed to colonize the gastric niche. Specific network motifs confer distinct transcriptional response dynamics to the TRN, while long regulatory cascades are absent. Rather than having a plethora of specialized regulators, the TRN of H. pylori appears to transduce separate environmental inputs by using different combinations of a small set of regulators

Amphetamine-induced taste aversion learning in young and old F-344 rats following exposure to 56Fe particles

Exposure to 56Fe particles produces changes in dopaminergic function and in dopamine-dependent behaviors, including amphetamine-induced conditioned taste aversion (CTA) learning. Because many of these changes are characteristic of the changes that accompany the aging process, the present study was designed to determine whether or not there would be an interaction between age and exposure to 56Fe particles in the disruption of an amphetamine-induced CTA. One hundred and forty F-344 male rats 2-, 7-, 12-, and 16-months old, were radiated with 56Fe particles (0.25–2.00 Gy, 1 GeV/n) at Brookhaven National Laboratory. Three days following irradiation, the rats were tested for the effects of radiation on the acquisition of a CTA produced by injection of amphetamine (3 mg/kg, i.p.). The main effect of age was to produce a significant decrease in conditioning day sucrose intake; there was no affect of age on the acquisition of the amphetamine-induced CTA. Exposing rats to 56Fe particles disrupted the acquisition of the CTA produced by injection of amphetamine only in the 2-month-old rats. These results do not support the hypothesis of an interaction between age and exposure to 56Fe particles in producing a disruption of amphetamine-induced CTA learning. As such, these results suggest that the aging produced by exposure to 56Fe particles may be endpoint specific