Fig. 2: Recovery of paternal gut microbiota rescues susceptibility to F1 phenotypes.
From: Paternal microbiome perturbations impact offspring fitness
a,b, Growth curves of F1 offspring sired by males during a time course of nABX withdrawal which still retain gut microbiota dysbiosis (6 wk + 4 rec) (a) and offspring of the same males after microbiota recovery (6 wk + 8 rec) (b), as well as aged-matched control sires. Line indicates mean, P value by nested (hierarchical) two-tailed t-test. c,d, Kaplan–Meier plot showing postnatal survival of F1 progeny sired by dysbiotic (c) or recovered nABX males (d). P value by Mantel–Cox (log-rank) test. e, Forest plots showing OR of F1 susceptibility to abnormal body weight and premature mortality when sired by dysbiotic (6 wk, 6 wk + 4 rec) or recovered males (6wk + 8 rec). Null effect is represented by a vertical line for which the OR value is 1. Whiskers indicate 95% CI, P value by two-sided Chi-square test (mortality: 6 wk P = 0.0001, 6 wk + 4 rec P = 0.0014, 6 wk + 8 rec P = 0.76; SGR: 6 wk P = 0.044, 6 wk + 4 rec P = 0.020, 6 wk + 8 rec P = 0.99). f, PCA of transcriptomes from F1 SGR adipose tissue sired by 6 wk or 6 wk + 4 rec nABX or control males, each from several independent litters. g, Gut microbiota richness of offspring (left) is not affected by paternal gut microbial status and does not correlate with F1 phenotype. Paternal microbiota richness (right) does correlate with F1 offspring phenotype. Shaded areas indicate 95% CI. h,i, Left, neonatal F1 body weight following IVF of isogenic oocytes using control or nABX-treated sperm donors. Right, F1 body-weight distribution at P15 following IVF. Data are independently derived from CD1 strain surrogate mothers (CON n = 66 offspring, nested into N = 12 fathers; nABX n = 75, nested into N = 12) (h) or BL6 strain surrogate mothers (CON n = 33 offspring, nested into N = 8 fathers; nABX n = 41, N = 7 fathers) (i). P value by nested (hierarchical) two-tailed t-test.
