Ontology highlight
ABSTRACT:
PROVIDER: PRJNA512033 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8375601_1.fastq.gz | Fastqsanger.gz | |||
| SRR8375601_2.fastq.gz | Fastqsanger.gz | |||
| SRR8375602_1.fastq.gz | Fastqsanger.gz | |||
| SRR8375602_2.fastq.gz | Fastqsanger.gz | |||
| SRR8375603_1.fastq.gz | Fastqsanger.gz |
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Project description:Whether myogenesis is affected by the maternal gut dysbacteriosis still remains ambiguous. In this study, firstly we show elevated level of lipopolysaccharides (LPS) in a gut microbiota dysbiosis mouse model. Secondly, we demonstrate that the diameter of muscle fibres, limb development and somitogenesis were inhibited in both gut microbiota dysbiosis and LPS exposed mice and chicken embryos. These might be due to LPS disturbed the cell survival and the key genes which regulating the somitogenesis and myogenesis. RNA sequencing and subsequent validation experiments verified that retinoic acid (RA) signaling perturbation was mainly responsible for the aberrant somite formation and differentiation. Subsequently, we found that LPS-induced Roxidative stress (ROS generation and antioxidant genes such as Nrf2, AKR) contributed to the above-mentioned interference with RA signaling. These findings highlight that the gut microbiota homeostasis also involved in regulating the development of muscle progenitor cells during pregnancy.
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