Source
Campbell, Łukasik, Meyer, Buckner, Simon, Veloso, Michalik & McCutcheon (2018), mBio 9(6): e02104-18, LIT-1590, read in full in NOTE-1235 from the PubMed Central copy (PMC6234865). The four results subsections, the discussion, Figures 1–4 from their captions, Table 1, and the methods with their caveats.
What was actually shown
- The problem, by simulation (Fig. 1). With random transmission, the cells needed to give every egg every lineage grow steeply with lineage number and unevenness, “by more than 2,000-fold” at Magicicada’s complexity. The authors call this an upper bound.
- Titres (Fig. 2). Four species, five or six eggs each, counted by
FISH and confocal microscopy.
- Hodgkinia: 4,889 (T. ulnaria, one lineage) to 30,154 (M. septendecim, many), about 6-fold. Only M. septendecim differs significantly from the others. T. chilensis (six lineages, about 12,000) does not.
- Sulcia: 2,572 to 5,643, about 2-fold, and if anything lower in M. septendecim.
- Transmission complete (Fig. 3). Every sampled egg of T. chilensis and T. limbata carried every rpoB lineage, and every M. septendecim egg carried both universal etfD genotypes. Eggs of one nest share their mother’s lineage proportions.
- Route unchanged (Fig. 4). The same stages under light microscopy in T. lacertosa and M. septendecim, with more cells migrating in Magicicada.
What could have failed: the Hodgkinia titre could have been the same across species, with complex cicadas laying eggs that lack lineages; or both symbionts’ titres could have risen together, pointing to a general change in the host’s transmission. Neither was found.
What this does not say
- Not a trend across complexity. One species of four carries the difference. One species stands for each level of complexity, and there is no phylogenetic control.
- Not that splitting came first. The authors raise the reverse, a high titre enabling splitting, and argue against it only because some cicadas keep an unsplit Hodgkinia.
- Not that no egg ever lacks a lineage. Presence was tracked by one or two marker genes, and the authors say rare losses could escape detection.
- Not that hosts do not sort lineages. Active sorting is untested.
- Not the feedback. That larger transmitted populations weaken host control and drive further splitting is, in the authors’ words, “speculative”.
Connections
- QUESTION-277. The one worked case in the record of host compensation at transmission. The host maintains reproductive cohesion (R) while the number of essential parts, and so dependence (D), grows. On the authors’ speculation, the same compensation may weaken host control (C) and selection alignment (S), which would make R and S trade off. The mapping to the dimensions is mine.
- CASE-177 is the case this account documents. The splitting it compensates for is reported in LIT-1563, LIT-1586, LIT-1612 and LIT-1602, all unread.
- THEORY-1049. The authors note that Hodgkinia cannot make its own membranes, so “the host must define Hodgkinia’s envelope”. That makes active sorting by the host conceivable. It is not shown.
Note of 2026-10-30: promoted, and the wider thesis filed beside it
The twenty-second status review promoted this reading under ADR-065: it reports what Campbell and colleagues measured and how they read it, and NOTE-1235 read the paper in full. Whether cicada hosts compensate for Hodgkinia’s splitting in general is THEORY-1214’s question, Proposed, which keeps this entry’s old promote_when.