Finding. A bloom-relevant sip of microcystin-LR (0.5 µg/L) does not write one ageing transcriptome in turquoise killifish. Old males and old females share only 27 differentially expressed genes. In that slim overlap, pck1 crashes and mitochondrial-function and metabolic genes move. Everywhere else the sexes diverge: male muscle contractile programs versus female egg-coat and vitellogenin programs. Cyanotoxin vulnerability in a senescent vertebrate is sex-shaped.
Why this paper matters
MC-LR literature is young-animal liver. This is old fish, low dose, whole-body, sex-split. The mitochondrial desk keeps the shared pck1/mitochondrial-function module and refuses to average the sexes.
What they actually measured
Whole-body RNA-seq, sex-stratified DE, shared versus unique programs, marker modules.
How to read the score
High fifties to low sixties. Score 61. Confidence is medium.
What to do with it
If you model ageing toxicology or cyanotoxins, split sex first and look at pck1. Do not infer a human advisory from 0.5 µg/L in killifish. The directional implication is that senescent males and females mount almost non-overlapping MC-LR programs around a small mitochondrial-metabolic core.