Additional file 5: Table S3. of Quinones are growth factors for the human gut microbiota

Quinone-induced bacteria have a disrupted menaquinone biosynthesis pathway, while related organisms not induced by quinones have a complete pathway. The genomes of the nearest type strains of all E. coli- or quinone-induced cultured bacteria were surveyed manually for the presence of a functional menaquinone biosynthesis pathway using a published dataset [24]. All organisms induced by E. coli or quinones in earlier co-culture experiments were missing large components of the menaquinone biosynthesis pathway, while Bacteroides species not induced by E. coli or quinones were predicted to have complete menaquinone biosynthetic capabilities. No strains were found to have predicted copies of genes in the futalosine pathway, an alternative means to generate menaquinone. ubiE/menG: 2-methoxy-6-polyprenyl-1,4-benzoquinol methylase; menF = Menaquinone-specific isochorismate synthase; menD = 2-succinyl-5-enolpyruvyl-6-hydroxy-3-cyclohexene-1-carboxylic-acid synthase; menH = 2-succinyl-6-hydroxy-2,4-cyclohexadiene-1-carboxylate synthase; menY = 2-succinyl-5-enolpyruvyl-6-hydroxy-3-cyclohexene-1-carboxylate dehydrogenase; menC = o-succinylbenzoate synthase; menE = o-succinylbenzoic acid--CoA ligase; menB = Naphthoate synthase. menI = 1,4-dihydroxy-2-naphthoyl-CoA hydrolase; menJ = 1,4-dihydroxy-2-naphthoyl-CoA hydrolasein (putative); menA = 1,4-dihydroxy-2-naphthoate polyprenyltransferase; mqnA = Chorismate dehydratase; mqnE = Aminodeoxyfutalosine synthase; mqnC = Cyclic dehypoxanthine futalosine synthase; mqnD = 1,4-dihydroxy-6-naphthoate synthase; mqnZ = 1,4-dihydroxy-6-naphthoate synthase (alternative); mqnX = Aminodeoxyfutalosine deaminase; mqnB = Futalosine hydrolase (EC 3.2.2.26); mtnN = Aminodeoxyfutalosine nucleosidase; mqnL = 1,4-dihydroxy-6-naphthoate carboxy-lyase, UbiD-like; mqnM = 2-heptaprenyl-1,4-naphthoquinone methyltransferase; mqnP = 1,4-naphthoquinone polyprenyltransferase. Data was taken and modified from Racheev, 2016. (XLSX 10 kb

Additional file 4: Figure S2. of Quinones are growth factors for the human gut microbiota

Single deletions in the E. coli menaquinone-8 pathway, but not ubiquinone-8 pathway, prevented growth induction of KLE1255. Single deletion mutants for all genes involved in ubiquinone-8 and menaquinone-8 biosynthesis were tested for induction capabilities of KLE1255. Red boxes indicate E. coli mutants with impaired growth induction capabilities for KLE1255. (PNG 364 kb

Additional file 6: Table S4. of Quinones are growth factors for the human gut microbiota

Quinone-dependent and control strains have predicted anaerobic reductases. The genomes of nearest type strains of all E. coli- or quinone-induced cultured bacteria were surveyed manually for the presence of individual annotated anaerobic reductases using a published dataset [35]. All analyzed organisms have the genetic capability to utilize anaerobic reductases for anaerobic respiration. Arx = Arsenate reductase; Cyd = Cytochrome bd reductase; Dms = Dimethyl sulfoxide reductase; Dsr = Sulfite reductase; Frd = Fumarate reductase; Nap = Nitrate reductase; Nar = Nitrate reductase; Nrf = Nitrite reductase; Phs = Thiosulfate reductase; Psr = Polysulfite reductase; Tor = Trimethylamine N-oxide reductase; Ttr = Tetrathionate reductase; Ynf = Selenate reductase. Data was taken and modified from Racheev, 2014 [35] and Ravcheev, 2016 [24]. (XLSX 8 kb

Additional file 3: Figure S1. of Quinones are growth factors for the human gut microbiota

Single deletions in the E. coli chorismate biosynthesis pathway prevented growth induction of KLE1255. Single deletion mutants for all genes involved in chorismate biosynthesis were tested for induction capabilities of KLE1255. Red boxes indicate E. coli mutants with impaired growth induction capabilities for KLE1255. (PNG 449 kb

Additional file 1: Table S1. of Quinones are growth factors for the human gut microbiota

Entire chromosome E. coli deletion library reformatted. 283 strains were first compiled from E. coli small-, medium-, and large-scale deletion libraries to cover all non-essential genes of the E. coli genome. Strains were taken from the Keio collection [19] and two larger deletion libraries [20, 21]. (XLS 36 kb

Additional file 2: Table S2. of Quinones are growth factors for the human gut microbiota

Strains identified in the E. coli knockout screen unable to induce the growth of KLE1255. Includes information on which genes are absent for each clone. (XLSX 18 kb

Unweighted UniFrac distances

The unweighted UniFrac distance (Lozupone and Knight AEM 2005) matrix of the 9511 fecal samples used in the American Gut paper. UniFrac was computed using Striped UniFrac (https://github.com/biocore/unifrac). Prior to execution of UniFrac, Deblur (Amir et al mSystems 2017) was run on the samples, all bloom sOTUs were removed (Amir et al mSystems 2017), and samples were rarefied to a depth of 1250 reads (Weiss et al Microbiome 2017). For the phylogeny, fragments were inserted using SEPP (Mirarab et al Pac Symp Biocomput 2012) into the Greengenes 13_5 99% OTU tree (McDonald et al ISME 2012)

movie_s1.mp4

Longitudinal samples from a large bowel resection. We place longitudinal samples collected prior to and following a large bowel resection in the context of samples from the AGP, the Earth Microbiome Project (https://www.ncbi.nlm.nih.gov/pubmed/29088705), intensive care unit patients (https://www.ncbi.nlm.nih.gov/pubmed/27602409), "extreme" diet samples from (https://www.ncbi.nlm.nih.gov/pubmed/24336217), and samples from the Hadza hunter-gatherers (https://www.ncbi.nlm.nih.gov/pubmed/28839072). Unweighted UniFrac was computed on this sample set, and principal coordinates were assessed. Using EMPeror (https://www.ncbi.nlm.nih.gov/pubmed/24280061), we then animate the plot by connect successive data points gut resection time series, while rotating the data frame. We first show the how the extent of change in the microbial community, and how the samples immediately following surgery resemble fecal samples from ICU patients. In the background of the animation, a black line connects a plant rhizosphere sample to a marine sediment sample, which have the same unweighted UniFrac distance (0.78) as the longitudinal sample immediately preceding and immediately following surgery

American Gut Project fecal sOTU counts table

The Deblur sOTU counts table for the fecal samples used in the American Gut Project manuscript. The samples were trimmed to a common read length of 125nt, and processed by Deblur (Amir et al mSystems 2017). Blooms were removed (Amir et al mSystems 2017) and any sample with fewer than 1250 sequences was omitted. This table is not rarefied,

movie_s2.mp4

Placing changes in the microbiome in the context of the American Gut. We accumulated samples over sequencing runs to demonstrate the structural consistency in the data. We demonstrate that while the ICU dataset (https://www.ncbi.nlm.nih.gov/pubmed/27602409) falls within the American Gut samples, they do not fall close to most samples at any of the body sites. We then highlight samples from the United Kingdom, Australia, the United States and other countries to show that nationality does not overcome the variation in body site. We then highlight the utility of the American Gut in meta-analysis by reproducing results from (https://www.ncbi.nlm.nih.gov/pubmed/20668239) and (https://www.ncbi.nlm.nih.gov/pubmed/23861384), using the AGP dataset as the context for dynamic microbiome changes instead of the HMP dataset. We show rapid, complete recovery of C. diff patients following fecal material transplantation and also contextualized the change in an infant gut over time until it settles into an adult state. This demonstrates the power of the American Gut dataset, both as a cohesive study and as a context for other investigations