The supplied author-citation record (h-index 2, 20 citations, papers on LSD perception, planetary defence, and DLR solar-furnace thermometry) is almost certainly a different person sharing the name: the OpenAlex profile matched to ORCID 0000-0003-3248-2772 shows 153 works, ~5,612 citations, h-index 34, and topics dominated by genetics and evolutionary biology β fully consistent with the HSP90 cavefish and single-cell atlas papers supplied. Per OpenAlex, this Rohner's citations peaked around 2013β2018, driven by the African coelacanth genome (~701 citations), the cavefish genome paper (~322), and the insulin-resistance cavefish Nature paper (~276). This review evaluates the evolutionary-genomics profile and flags the homonym risk explicitly rather than averaging two incompatible records.
The HSP90 capacitor study (Science, 2013) is the flagship: HSP90 inhibition (500 nM radicicol) increased eye-size SD by +58β83% and orbit-size SD by +108% in surface Astyanax mexicanus (Bartlett/Levene P < 0.001), while cave-like low conductivity mimicked the effect (+50β58% variation), and selection on treated lines produced heritable eye reduction without drug (P = 7.2e-16) β an unusually complete demonstration of buffering, release, and genetic assimilation in a natural population . His group then translated metabolic cave adaptations (MC4R mutations; insulin resistance) into clinically relevant diabetes biology . Most recently, a snRNA-seq/spatial atlas (117,000 nuclei, 35 clusters) maps cave-adaptation to coordinated circadian, HIF1A, immune, and glia-to-neuron signaling remodeling β observational but with a falsifiable pathway-level design and full data release (GEO GSE335564) .
Weaknesses are visible in the records: small samples in some assays (e.g., n=1 per group for hematopoietic flow cytometry in the Tol2 transgenesis paper) ; radicicol off-target effects; cross-species orthology projection in pathway interpretation; and inferred (not exhaustively demonstrated) causality between HSP90 buffering and natural eye loss. Funding is conventional NIH/NSF/institute support; one co-author on the HSP90 paper disclosed a consultant conflict, unrelated to the biology. Strengths: trait-level negative controls (dark rearing alone had no effect; body size and neuromasts showed no cryptic variation), appropriate variance tests, and a null-grouping control in the atlas (random grouping yielded only 3 DEGs). What would change the assessment: failure of independent labs to replicate the assimilation phenotype, or cell-number-driven artifacts in the immune atlas analyses.
Confidence: high on the evolutionary-genomics profile (multiple independent high-impact papers); low on the homonym-corrected metrics because the two supplied profiles conflict.
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