Thermal preconditioning shifts cell signaling in favor of
pro-life genes pBcl-2 and pBI-1
Expression of pro-survival genes pBI-1 and pBcl-2 and
pro-death genes pBAK and pBAX increased during first six
hours of the stress (Fig. 2A). After preconditioning, the increase of
pBI-1 , pBcl-2 and pBAX expression was even more
pronounced (p(BI-1,3h) = 0.006, p(Bcl-2,
0h) = 0.076, p(Bcl-2, 3h) = 0.002,
p(BAX, 1h) = 0.027, p(BAX, 3h) = 0.014),
but the expression of pro-death BAK gene in PC corals dropped to
control levels at 6 hours, differing from the NPC corals (p = 0.084).
Upon proper signaling, BAK and BAX heterodimerize and permeabilize
mitochondrial membrane, releasing cytochrome c and considerably
progressing towards cell death (Galluzzi et al., 2018; Karch et al.,
2017). Bcl-2 can antagonize this process via direct protein-protein
interaction with both BAK and BAX. BI-1 acts as an apoptosis inhibitor
but the exact mechanism is still not fully understood. PCD signaling
consists of a complex protein networking where single gene expression
profile does not reflect the entirety of the process. For this reason,
we calculated the expression ratio of pro-survival vs. pro-death genes
to better express the prevalent signalization in the cell. After
preconditioning, the pBcl/pBAK, pBcl/pBAX, and pBI/pBAX ratios shift
towards the pro-survival partner during the early heat-stress response
(Fig. 2B). pBI-1 expression level is higher than the pBAXexpression level in PC vs. NPC corals at the first hour after stress (p
= 0.058). pBcl-2 is expressed considerably more than the
pBAK gene at 3 hours (p = 0.002), while compared to pBAX ,
it’s the basal expression of pBcl-2 in non-stressed PC corals and
the expression around 1h of the stress that is higher
(p(0h) = 0.005, p(1h) = 0.084). All
these results suggest that during thermal preconditioning, coral PCD
signaling is manipulated to favor the pro-survival genes.