Telomere length in colonial corals records cumulative metabolic stress rather than mitotic cycles, suggesting it functions as a molecular ledger of holobiont information entropy. If telomeres store a readable signal of stress exposure, then interventions that reduce holobiont oxidative burden should not only slow telomere attrition but actively reset the telomeric state to a baseline associated with low‑stress conditions. We hypothesize that probiotic inoculation with Beneficial Microorganisms for Corals (BMCs) will trigger a reversible lengthening of telomeres in adult Polyps of Porites spp., mediated by upregulation of host telomerase reverse transcriptase (TERT) and downregulation of stress‑activated p53 pathways, and that this resetting will be detectable only when the microbiome shift persists for at least two weeks post‑heat stress.

To test this, we will fragment nubbins of Porites lobata and expose half to a standardized heat‑stress protocol (32 °C for 48 h) while the other half remains at ambient temperature (26 °C). Immediately after heat exposure, both sets will receive either a BMC cocktail (isolated from healthy Porites, comprising Endozoicomonas spp. and Halomonas spp.) or a seawater control. Telomere length will be measured by quantitative PCR (qPCR) at 0 h, 7 d, 14 d, and 28 d post‑treatment. Parallel assays will quantify host TERT transcript levels, p53‑target gene expression, and reactive oxygen species (ROS) concentrations in the tissue.

We predict three outcomes: (1) Heat‑stressed nubbins receiving BMCs will show a statistically significant increase in telomere length relative to heat‑stressed controls by day 14, approaching the lengths of non‑stressed baselines; (2) This lengthening will correlate with a ≥2‑fold rise in TERT mRNA and a ≥50 % reduction in p53‑target transcripts; (3) In the absence of sustained BMC presence (i.e., after microbiome washout at day 7), telomere length will resume its shortening trajectory, indicating that the reset is contingent on ongoing microbiome‑mediated metabolic remodeling.

A falsifiable alternative is that BMCs merely protect telomeres from further shortening without inducing lengthening; in that case, telomere trajectories would remain flat or only marginally improved, and TERT expression would not rise above baseline. Demonstrating active telomere resetting would extend the stress‑integration model to a dynamic information‑storage system where the holobiont microbiome can edit the telomeric ledger, linking environmental memory to cellular aging mechanisms in a clonal, long‑lived invertebrate.