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Legionella pneumophila is a gram‐negative bacteria found in natural and anthropogenic aquatic environments such as evaporative cooling towers, where it reproduces as an intracellular parasite of cohabiting protozoa. If L. pneumophila is aerosolized and inhaled by a susceptible person, bacteria may colonize their alveolar macrophages causing the opportunistic pneumonia Legionnaires' disease. L. pneumophila utilizes an elaborate regulatory network to control virulence processes such as the Dot/Icm Type IV secretion system and effector repertoire, responding to changing nutritional cues as their host becomes depleted. The bacteria subsequently differentiate to a transmissive state that can survive in the environment until a replacement host is encountered and colonized. In this review, we discuss the lifecycle of L. pneumophila and the molecular regulatory network that senses nutritional depletion via the stringent response, a link to stationary phase‐like metabolic changes via alternative sigma factors, and two‐component systems that are homologous to stress sensors in other pathogens, to regulate differentiation between the intracellular replicative phase and more transmissible states. Together, we highlight how this prototypic intracellular pathogen offers enormous potential in understanding how molecular mechanisms enable intracellular parasitism and pathogenicity. [ABSTRACT FROM AUTHOR]

Quorum sensing among gram-negative bacteria is an important component of biofilm production. This is done via the production of acylated homoserine lactone molecules, which in Pseudomonas aeruginosa are produced by the las and rhl genes.

Focuses on a study where researchers aimed to clone and characterize genes involved in core biosynthesis. Reference to completed studies on the issue; Methodology used in the experiment; Results of the experiment; Implications of the results; Benefits of the study.

Discusses the monoclonal antibodies (MAB) that distinguish inner core, outer core, and lipid A regions of the Pseudomonas aeuginosa lipopolysaccharide (LPS). Isolation of this bacteria; Serotypes determined; Western immunoblots of LPS; Potential of MAbs 101 and 7-4 for detection of the organism.

Previous work from our laboratory has shown that cosmid clone pFV100, containing a 26 kb insert, is able to restore O-antigen synthesis in serotype 05 rough mutants of Pseudomonas aeruginosa. Mobilization of pFV100 into two P. aeruginosa semi-rough (SR) mutants, AK1401 and rd7513, resulted in O-antigen expression, indicating that pFV100 may contain an 0-polymerase (rfc) gene. pFV.TK6, a subclone of pFV100 that contains a 5.6kb chromosomal insert. was able to complement O-antigen expression in these SR mutants. Mutagenesis of pFV.TK6 using Tn 1000 exposed a 1.5 kb region that was essential for complementing O-antigen expression in AK1401. A 20 kb Xhol-Hindlll fragment, containing this region, was cloned into vector pUCP26 and the resulting plasmid called pFV.TK8. In Southern analysis of the 20 P. aeruginosa serotypes using a probe generated from the 1.5 kb Xhol fragment of pFV.TK8, the rfc probe hybridized to a common fragment of the cross-reactive 02-05-016-018-020 serogroup, suggesting that these serotypes may share a common O-polymerase gene. In functional studies of the rfc gene, the PA01 (serotype 05) chromosomal rfc was mutated using a gene-replacement strategy. These knockout mutants expressed the SR lipopolysaccharide (LPS) phenotype, which indicated that they were no longer producing a functional 0-polymerase enzyme. Nucleotide sequence analysis of the insert DNA of pFV.TK8 revealed one open reading frame (ORF), designated ORF48.9, which could code for a 48.9 kDa protein. In comparisons of the P. aeruginosa rfc nucleotide and amino acid sequences with DNA and protein databases, no significant homology was found. However, the deduced structure of the P. aeruginosa Rfc protein indicated that it is very hydro-phobic and contains 11 putative membrane-spanning domains. Therefore, the predicted structure is similar to that of other reported Rfc... [ABSTRACT FROM AUTHOR]

White mold is caused by the fungal pathogen Sclerotinia sclerotiorum and leads to rapid and significant loss in plant yield. Among its many brassicaceous hosts, including Brassica napus (canola) and Arabidopsis, the response of individual tissue layers directly at the site of infection has yet to be explored. Using laser microdissection coupled with RNA sequencing, we profiled the epidermis, mesophyll, and vascular leaf tissue layers of B. napus in response to S. sclerotiorum. High-throughput tissue-specific mRNA sequencing increased the total number of detected transcripts compared with whole-leaf assessments and provided novel insight into the conserved and specific roles of ontogenetically distinct leaf tissue layers in response to infection. When subjected to pathogen infection, the epidermis, mesophyll, and vasculature activate both specific and shared gene sets. Putative defense genes identified through transcription factor network analysis were then screened for susceptibility against necrotrophic, hemi-biotrophic, and biotrophic pathogens. Arabidopsis deficient in PR5-like RECEPTOR KINASE (PR5K) mRNA levels were universally susceptible to all pathogens tested and were further characterized to identify putative interacting partners involved in the PR5K signaling pathway. Together, these data provide insight into the complexity of the plant defense response directly at the site of infection., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email: journals.permissions@oup.com.)