Figure 2.

Statistical Data Showed Protective Role of PRL-1 in Nervous System against CO₂ Insult

(A) Neuronal-specific expression of PRL-1 (elav-GAL4) in the mutants completely rescued the wing held-up phenotype induced by CO₂, but expression in other tissues such as muscles (Mhc-GAL4) or glial cells (repo-GAL4) did not result in any rescue.

(B) The response of PRL-1 mutant flies to alternative anesthetics, such as carbon dioxide (CO₂), ether, and nitrogen (N₂). Permanent wing phenotype was only induced by CO₂.

(C) In the PRL-1 mutant background, knockdown of CO₂ sensory receptor protein Gr21a driven by Gr63a-GAL4 prevented the wing phenotype.

(D) Within the transition time (about 10 min) when flies were shifted from non-permissive temperature (29°C) back to the permissive temperature (25°C), the vast majority of flies ectopically expressed shi^ts1 in the nervous system (elav-GAL4>UAS-shi^ts1) and exhibited a transient wing held-up phenotype. A similar wing phenotype was also observed when shi^ts1was specifically expressed in motor neurons (D42-GAL4>UAS-shi^ts1).

Data are expressed as mean ± SD. *p < 0.05, ***p < 0.001. See also Figures S2 and S4.