RESUMEN
Environmental stressors can impact the basic biology and applications of host-microbe symbioses. For example, Wolbachia symbiont densities and cytoplasmic incompatibility (CI) levels can decline in response to extreme temperatures and host aging. To investigate whether transgenic expression of CI-causing cif genes overcomes the environmental sensitivity of CI, we exposed transgenic male flies to low and high temperatures as well as aging treatments. Our results indicate that transgenic cif expression induces nearly complete CI regardless of temperature and aging, despite severe weakening of Wolbachia-based wild-type CI. Strong CI levels correlate with higher levels of cif transgene expression in young males. Altogether, our results highlight that transgenic CI persists against common environmental pressures and may be relevant for future control applications involving the cifA and cifB transgenes.
RESUMEN
Early-life antibiotic exposure perturbs the intestinal microbiota and accelerates type 1 diabetes (T1D) development in the NOD mouse model. Here, we found that maternal cecal microbiota transfer (CMT) to NOD mice after early-life antibiotic perturbation largely rescued the induced T1D enhancement. Restoration of the intestinal microbiome was significant and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed metabolites and normalized innate and adaptive immune effectors. CMT restored major patterns of ileal microRNA and histone regulation of gene expression. Further experiments suggest a gut-microbiota-regulated T1D protection mechanism centered on Reg3γ, in an innate intestinal immune network involving CD44, TLR2, and Reg3γ. This regulation affects downstream immunological tone, which may lead to protection against tissue-specific T1D injury.
