Fig. 3. Integrative model of the genes and pathways of larvae of Acropora digitifera involved in the interaction with Chromera.

Upregulated and downregulated genes/functions are in blue and red text, respectively. The initial contact phase (left panel) involves upregulation of ribosomal and mitochondrial functions (based on enrichment of GO terms), and suppression of host immune responses including the downregulation of the pattern recognition receptors (PRRs) that can recognize signature microbial compounds (i.e., microbe-associated molecular patterns or MAMPs). The PRRs that were detected included toll-like receptors (TLRs), a nucleotide-binding oligomerization domain (Nod) protein, scavenger receptors (SRs), lectins, and the complement protein C3. Moreover, the pancreatic secretory granule membrane major glycoprotein GP2, which serves as an uptake receptor for pathogenic bacteria in man, was strongly downregulated. Suppression of PRR–MAMP interactions leads to inactivation of nuclear factor kappa-B (NF-kappa-B), which is a master regulator of immunity. The phagosome formation phase (central panel) involves downregulation of genes involved in phagocytosis and actin remodeling as well as differential expression of genes implicated in endosomal trafficking that enhance the maturation of the phagosome and lysosome fusion (see Fig. 4 for more details about those genes). The Chromera tolerance phase (right panel) involves complex changes in the apoptotic network. During this phase, genes likely to have both anti-apoptotic and pro-apoptotic functions were differentially expressed