Multiple factors over the lifetime of an individual, including diet, geography, and physiologic state, will influence the microbial communities within the primate gut. To determine the source of variation in the composition of the microbiota within and among species, we investigated the distal gut microbial communities harbored by great apes, as present in fecal samples recovered within their native ranges. We found that the branching order of host-species phylogenies based on the composition of these microbial communities is completely congruent with the known relationships of the hosts. Although the gut is initially and continuously seeded by bacteria that are acquired from external sources, we establish that over evolutionary timescales, the composition of the gut microbiota among great ape species is phylogenetically conserved and has diverged in a manner consistent with vertical inheritance. The microbial communities that inhabit the gastrointestinal tract of humans and other mammals are complex, dynamic, and critical to both health and disease. The composition and constituents of these communities are influenced by multiple factors such as host diet, geography, physiology, and disease state. Given the central role of the gut microbiota in the physiology of the host, it is important to determine whether it is predictable and substantially determined by the host, or variable and largely determined by the external environment (including diet) experienced by the host. A valuable way of determining the relative contributions of such factors is by comparing gut microbial communities in closely related host species. Applying a high-throughput sequencing approach, we profiled the distal gut microbiotae of great ape species sampled in their native ranges and then employed a parsimony-based analysis of phylogenetically informative phylotypes (i.e., bacterial taxa residing in multiple individuals) to determine the relationships among the diverse microbial communities. Our analyses revealed a clear species-specific signature of microbial community structure. Moreover, the pattern of relationships among the five great ape species (Homo sapiens, Pan troglodytes, P. paniscus, Gorilla gorilla, and G. beringei) inferred from their fecal microbial communities was identical to that inferred from host mitochondrial DNA, indicating that host phylogeny shapes the gut microbiota over evolutionary timescales. It seems after all that you are not what you eat.

Genetic drift, which is particularly effective within small populations, can shape the size and complexity of genomes by affecting the fixation of deleterious mutations. In Bacteria, assessing the contribution of genetic drift to genome evolution is problematic because the usual methods, based on intraspecific polymorphisms, can be thwarted by difficulties in delineating species' boundaries. The increased availability of sequenced bacterial genomes allows application of an alternative estimator of drift, the genome-wide ratio of replacement to silent substitutions in protein-coding sequences. This ratio, which reflects the action of purifying selection across the entire genome, shows a strong inverse relationship with genome size, indicating that drift promotes genome reduction in bacteria.

Elevated levels of genetic drift are hypothesized to be a dominant factor that influences genome size evolution across all life-forms. However, increased levels of drift appear to be correlated with genome expansion in eukaryotes but with genome contraction in bacteria, suggesting that these two groups of organisms experience vastly different mutational inputs and selective constraints. To determine the contribution of small insertion and deletion events to the differences in genome organization between eukaryotes and prokaryotes, we systematically surveyed 17 taxonomic groups across the three domains of life. Based on over 5,000 indel events in noncoding regions, we found that deletional events outnumbered insertions in all groups examined. The extent of deletional bias, when measured by the total length of insertions to deletions, revealed a marked disparity between eukaryotes and prokaryotes, whereas the ratio was close to one in the three eukaryotic groups examined, deletions outweighed insertions by at least a factor of 10 in most prokaryotes. Moreover, the strength of deletional bias is associated with the proportion of coding regions in prokaryotic genomes. Considering that genetic drift is a stochastic process and does not discriminate the exact nature of mutations, the degree of bias toward deletions provides an explanation to the differential responses of eukaryotes and prokaryotes to elevated levels of drift. Furthermore, deletional bias, rather than natural selection, is the primary mechanism by which the compact gene packing within most prokaryotic genomes is maintained.

Type VI secretion system (T6SS) is a macromolecular machine used by many Gram-negative bacteria to inject effectors/toxins into eukaryotic hosts or prokaryotic competitors for survival and fitness. To date, our knowledge of the molecular determinants and mechanisms underlying the transport of these effectors remains limited. Here, we report that two T6SS encoded valine-glycine repeat protein G (VgrG) paralogs in Agrobacterium tumefaciens C58 specifically control the secretion and interbacterial competition activity of the type VI DNase toxins Tde1 and Tde2. Deletion and domain-swapping analysis identified that the C-terminal extension of VgrG1 specifically confers Tde1 secretion and Tde1-dependent interbacterial competition activity in planta, and the C-terminal variable region of VgrG2 governs this specificity for Tde2. Functional studies of VgrG1 and VgrG2 variants with stepwise deletion of the C terminus revealed that the C-terminal 31 aa (C31) of VgrG1 and 8 aa (C8) of VgrG2 are the molecular determinants specifically required for delivery of each cognate Tde toxin. Further in-depth studies on Tde toxin delivery mechanisms revealed that VgrG1 interacts with the adaptor/chaperone–effector complex (Tap-1–Tde1) in the absence of proline-alanine-alanine-arginine (PAAR) and the VgrG1–PAAR complex forms independent of Tap-1 and Tde1. Importantly, we identified the regions involved in these interactions. Although the entire C31 segment is required for binding with the Tap-1–Tde1 complex, only the first 15 aa of this region are necessary for PAAR binding. These results suggest that the VgrG1 C terminus interacts sequentially or simultaneously with the Tap-1–Tde1 complex and PAAR to govern Tde1 translocation across bacterial membranes and delivery into target cells for antibacterial activity. Significance The type VI secretion system involves multiple strategies for effector delivery via fusion or interaction of effectors to structural components of the phage tail-like structure, the tube component Hcp or spike protein VgrG. However, the detailed mechanisms underlying how diverse VgrG proteins govern effector delivery remains unclear. Here, we report that the divergent C-terminus of VgrG protein is the molecular determinant governing specific effector delivery and is required for interacting with a specific adaptor/chaperone protein that stabilizes and binds directly with the cognate effector. The striking conservation of genetic modules encoding homologous VgrG, a distinct set of potential adaptor/chaperone, and a specific effector in various Proteobacteria strongly suggest a conserved mechanism in type VI effector delivery.

The genus ‘Candidatus Phytoplasma’ was proposed to accommodate cell wall-less bacteria that are molecularly and biochemically incompletely characterized, and colonize plant phloem and insect vector tissues. This provisional classification is highly relevant due to its application in epidemiological and ecological studies, mainly aimed at keeping the severe phytoplasma plant diseases under control worldwide. Given the increasing discovery of molecular diversity within the genus ‘Ca. Phytoplasma’, the proposed guidelines were revised and clarified to accommodate those ‘Ca. Phytoplasma’ species strains sharing >98.65 % sequence identity of their full or nearly full 16S rRNA gene sequences, obtained with at least twofold coverage of the sequence, compared with those of the reference strain of such species. Strains sharing 98.65 % with other strain(s) within the same ‘Ca. Phytoplasma’ species should be considered related strains to that ‘Ca. Phytoplasma’ species. The guidelines herein, keep the original published reference strains. However, to improve ‘Ca. Phytoplasma’ species assignment, complementary strains are suggested as an alternative to the reference strains. This will be implemented when only a partial 16S rRNA gene and/or a few other genes have been sequenced, or the strain is no longer available for further molecular characterization. Lists of ‘Ca. Phytoplasma’ species and alternative reference strains described are reported. For new ‘Ca. Phytoplasma’ species that will be assigned with identity ≥98.65 % of their 16S rRNA gene sequences, a threshold of 95 % genome-wide average nucleotide identity is suggested. When the whole genome sequences are unavailable, two among conserved housekeeping genes could be used. There are 49 officially published ‘Candidatus Phytoplasma’ species, including ‘Ca. P. cocostanzaniae’ and ‘Ca. P. palmae’ described in this manuscript.

Certain obligate parasites induce complex and substantial phenotypic changes in their hosts in ways that favor their transmission to other trophic levels. However, the mechanisms underlying these changes remain largely unknown. Here we demonstrate how SAP05 protein effectors from insect-vectored plant pathogenic phytoplasmas take control of several plant developmental processes. These effectors simultaneously prolong the host lifespan and induce witches’ broom-like proliferations of leaf and sterile shoots, organs colonized by phytoplasmas and vectors. SAP05 acts by mediating the concurrent degradation of SPL and GATA developmental regulators via a process that relies on hijacking the plant ubiquitin receptor RPN10 independent of substrate ubiquitination. RPN10 is highly conserved among eukaryotes, but SAP05 does not bind insect vector RPN10. A two-amino-acid substitution within plant RPN10 generates a functional variant that is resistant to SAP05 activities. Therefore, one effector protein enables obligate parasitic phytoplasmas to induce a plethora of developmental phenotypes in their hosts.