Campbell, M. A., Łukasik, P., Meyer, M. C., Buckner, M., Simon, C., Veloso, C., Michalik, A. & McCutcheon, J. P. (2018). Changes in Endosymbiont Complexity Drive Host-Level Compensatory Adaptations in Cicadas. mBio 9(6): e02104-18. doi:10.1128/mBio.02104-18.
Key takeaways
From the reading, NOTE-1235.
- The problem. With random transmission, the cells needed to give every egg every Hodgkinia lineage grow steeply as lineages multiply and grow uneven: over 500 per egg for one cell of each of T. chilensis’s six lineages, 4 to 5 times more at Magicicada’s complexity.
- The host’s answer. Hodgkinia cells per egg range from 4,889 in a single-lineage cicada to 30,154 in M. septendecim; Sulcia stays between 2,572 and 5,643. Only M. septendecim differs significantly (THEORY-1106).
- Transmission complete. Every sampled egg carried every tracked lineage, and eggs share their mother’s lineage proportions. Rare losses could escape detection, the authors say.
- Same route. Under the light microscope, transmission looks the same in a three-lineage Tettigades and in Magicicada.
- A possible feedback. Larger transmitted populations mean weaker bottlenecks, which the authors speculate could reduce host control and feed further splitting.
Why this is here
A2 listed “host compensation” (“selection to maintain collective functionality”, giving “transport, regulation, or metabolic rescue”) as a mechanism, and named no work for it. This is a documented case of the host compensating at the level of transmission, so it bears on reproductive cohesion (R) in QUESTION-277. The reading finds that the host maintains cohesion as the parts multiply, rather than raising it, and that the authors suspect the same change may weaken the host’s control. Registered for CASE-177.