Abstract
The mytilid mussel Bathymodiolus thermophilus lives in the deep-sea hydrothermal vent regions due to its relationship with chemosynthetic symbiotic bacteria. It is well established that symbionts reside in the gill bacteriocytes of the mussel and can utilize hydrogen sulfide, methane, and hydrogen from the surrounding environment. However, it is observed that some mussel symbionts either possess or lack genes for hydrogen metabolism within the single-ribotype population and host mussel species level. Here, we found a hydrogenase cluster consisting of additional H2-sensing hydrogenase subunits in a complete genome of B. thermophilus symbiont sampled from an individual mussel from the East Pacific Rise (EPR9N). Also, we found methylated regions sparsely distributed throughout the EPR9N genome, mainly in the transposase regions and densely present in the rRNA gene regions. CRISPR diversity analysis confirmed that this genome originated from a single symbiont strain. Furthermore, from the comparative analysis, we observed variation in genome size, gene content, and genome re-arrangements across individual hosts suggesting multiple symbiont strains can associate with B. thermophilus. The ability to acquire locally adaptive various symbiotic strains may serve as an effective mechanism for successfully colonizing different chemosynthetic environments across the global oceans by host mussels.
Original language | English |
---|---|
Article number | 22232 |
Journal | Scientific Reports |
Volume | 12 |
Issue number | 1 |
DOIs | |
State | Published - Dec 2022 |
Bibliographical note
Funding Information:We are grateful to Dr. Robert C. Vrijenhoek for providing B. thermophilus sample from EPR9N hydrothermal vent. This research was supported by a grant (No. PE9988B and PEA0083) of Korea Institute of Ocean Science & Technology, KIOST, and was part of a project titled ‘Understanding the deep-sea biosphere on seafloor hydrothermal vents in the Indian Ridge (No. 20170411)’ funded by the Ministry of Oceans and Fisheries, Korea.
Publisher Copyright:
© 2022, The Author(s).