Microbial Genetic Composition Tunes Host Longevity

Abstract

Our paper reported a telomere cap exchange process during meiosis. During the preparation of Figure 2D, we miscalculated the number of cells for each developmental substage (namely Lep, Zyg, and Pac), in which the TRF1 foci numbers were reported. It was stated in the figure legend that more than 30 cells were analyzed for each substage; however, this statement was inaccurate and incorrect. For clarification, we have provided a revised version of Figure 2 showing the number of cells we analyzed for different substages with each genetic background. This error does not affect the results in the paper or the interpretation of the data. We apologize for any confusion this error may have caused.

Structural variation in the gut microbiome associates with host health

“…Genes that are deleted or duplicated within different members of a species (also termed copy number variation; CNV), are a phenomenon common across all kingdoms of life 1,2 . Even a small number of bacterial genes can underlie phenotypes such as virulence 3 , antibiotic resistance 4 , host metabolic disease 5 , and host longevity 6 , making genetic variation highly important to both the microbe and its host.…”

The Preliminary Development of an in vitro Poultry Cecal Culture Model to Evaluate the Effects of Original XPCTM for the Reduction of Campylobacter jejuni and Its Potential Effects on the Microbiota

“…One approach to controlling Campylobacter pre-harvest is by influencing the gut microbiome with various probiotic, prebiotic, enzyme, and fermentate compounds to promote the competitive exclusion of Campylobacter and the fortification of the host immunobiology-microbiome axis (Baffoni et al, 2012;Guyard-Nicodème et al, 2016;Schneitz and Hakkinen, 2016). Specifically, yeast fermentates likely promote changes to the microbiome that are theorized to aid in the stability of the host-immunobiology axis (Possemiers et al, 2013;Han et al, 2017). Evidence also suggests that the microbiota dictates both the window of opportunity for Campylobacter colonization in poultry, while also aiding in the TH 1 immune response polarization to control Campylobacter colonization (Han et al, 2017).…”

“…Specifically, yeast fermentates likely promote changes to the microbiome that are theorized to aid in the stability of the host-immunobiology axis (Possemiers et al, 2013;Han et al, 2017). Evidence also suggests that the microbiota dictates both the window of opportunity for Campylobacter colonization in poultry, while also aiding in the TH 1 immune response polarization to control Campylobacter colonization (Han et al, 2017). Previous research by our group and others demonstrated that the Saccharomyces cerevisiae fermentate Original XPC TM (XPC; Diamond V, Cedar Rapids, IA, United States) inhibits Salmonella Typhimurium, both in an in vitro anaerobic mixed culture assay and in vivo (Feye et al, 2016;Rubinelli et al, 2016;Roto et al, 2017).…”

Bacteria increase host micronutrient availability: mechanisms revealed by studies in C. elegans

“…Lifespan extension on pabB, aroD, and aroG was found to be dependent on the C. elegans gene rict-1, which encodes a component of the target of rapamycin complex 2 (TORC2), known to interact with the insulin signaling pathway and integrate nutritional signals to extend lifespan [47]. Lifespan was not dependent on eat-2 or daf-16, thus ruling out dietary restriction as a mechanism for lifespan increase [46]. No further investigation was carried out into the interaction of bacterial folates with TORC2, and the mechanism underpinning how folate acts as a nutritional signal to C. elegans is unclear.…”

“…The THF precursors, para-aminobenzoic acid (PABA) (synthesized from chorismate and glutamine), and pteridine (synthesized from GTP) are conjugated to form dihydropteroate, which is glutamylated and reduced to form THF. THF derivatives are generated by the acceptance and transfer of one-carbon units in reactions that facilitate cellular biosynthesis and methylation reactions aging [45,46]. Of the nine genes isolated in the Virk et al screen, two were involved in folate synthesis (pabA and pabB) and three (pabB, aroD, aroG) of the 29 isolated in the Han et al screen.…”