Shedding light on bacteria-host interactions with the aid of TnSeq approaches

Abstract

Bacteria are highly adaptable and grow in diverse niches, where they often interact with eukaryotic organisms. These interactions with different hosts span the entire spectrum from symbiosis to pathogenicity and thus determine the lifestyle of the bacterium. Knowledge of the genetic determinants involved in animal and plant host colonization by pathogenic and mutualistic bacteria is not only crucial to discover new drug targets for disease management but also for developing novel biostimulant strategies. In the last decades, significant progress in genome-wide high-throughput technologies such as transposon insertion sequencing has led to the identification of pathways that enable efficient host colonization. However, the extent to which similar genes play a role in this process in different bacteria is yet unclear. This review highlights the commonalities and specificities of bacterial determinants important for bacteria-host interaction.

Keywords: colonization; fitness genes; host–bacteria interactions; transposon sequencing.

Fig 1

Overview of cell functions involved in host colonization. Examples shown include motility toward/away the host and its metabolites, tolerance to host-related stresses and defense mechanisms, metabolism of available energy sources in the host, attachment, intracellular invasion, and competition/synergy with other host microorganisms, among others.

Fig 2

Use of TnSeq to assess gene function. (A) Outline of the TnSeq workflow. (B) TnSeq studies published per year since 2009. Data were downloaded from the Web of Science (date of search: 1 June 2023) and curated manually. In orange, in vivo animal host TnSeq studies. In green, in vivo plant host TnSeq studies. In yellow, other types of TnSeq studies (essential genome identification, in vitro, ex vivo models, protocols, analysis tools, reviews, etc.). (C) Number of different bacterial phyla targeted in in vivo plant host studies, in vivo animal host studies, and other type of TnSeq studies. The data used to construct these graphs were curated manually and can be found in Table S1.

Fig 3

Overview of genes providing a fitness benefit for different interactions of bacteria with plant and animal hosts. (A) Percentage of genes for each COG categories identified as important for colonization of animal and plant hosts. For illustration purposes, square root of percentage values is presented. (B) Identification of genes required for purine biosynthesis (purABCDEFHKLMN) and tryptophan metabolism (trpABCDEFGHRS and aroABCEGQ) as important (grey) for host colonization in the different species. White color means no genes of the pathway were found to be important for colonization in the corresponding TnSeq study. (C) Average percentage of genes in each COG category involved in colonization, according to type of host and type of interaction. For illustration purposes, COG category S (corresponding to function unknown) is not shown. (D) Difference between average percentages of genes in each COG category involved in colonization, according to type of host and type of interaction. COG categories description: A = RNA processing and modification; B = chromatin structure and dynamics; C = energy production and conversion; D = cell cycle control, cell division, and chromosome partitioning; E = amino acid transport and metabolism; F = nucleotide transport and metabolism; G = carbohydrate transport and metabolism; H = coenzyme transport and metabolism; I = lipid transport and metabolism; J = translation, ribosomal structure, and biogenesis; K = transcription; L = replication, recombination, and repair; M = cell wall, membrane, and envelope biogenesis, N = cell motility, O = post-translational modification, protein turnover, and chaperonesl; P = inorganic ion transport and metabolism; Q = secondary metabolites biosynthesis, transport, and catabolism; S = function unknown; T = signal transduction mechanisms; U = intracellular trafficking, secretion, and vesicular transport; V = defense mechanisms.