Role of mef2ca in developmental buffering of the zebrafish larval hyoid dermal skeleton

Phenotypic robustness requires a process of developmental buffering that is largely not understood, but which can be disrupted by mutations. Here we show that in mef2cab1086 loss of function mutant embryos and early larvae, development of craniofacial hyoid bones, the opercle (Op) and branchiostegal ray (BR), becomes remarkably unstable; the large magnitude of the instability serves as a positive attribute to learn about features of this developmental buffering. The OpBR mutant phenotype variably includes bone expansion and fusion, Op duplication, and BR homeosis. Formation of a novel bone strut, or a bone bridge connecting the Op and BR together occurs frequently. We find no evidence that the phenotypic stability in the wild type is provided by redundancy between mef2ca and its co-ortholog mef2cb, or that it is related to the selector (homeotic) gene function of mef2ca. Changes in dorsal–ventral patterning of the hyoid arch also might not contribute to phenotypic instability in mutants. However, subsequent development of the bone lineage itself, including osteoblast differentiation and morphogenetic outgrowth, shows marked variation. Hence, steps along the developmental trajectory appear differentially sensitive to the loss of buffering, providing focus for the future study. •Opercle and branchiostegal ray hyoid bones are variably expanded and fused in mef2ca mutants.•Expanded bone phenotypes arise from ectopic osteoblast differentiation in mutants.•The ectopic bone exhibits opercle identity as well as novel morphological features.•Loss of mef2ca causes disruption of developmental buffering producing developmental instability.•Stability is not due to redundancy with mef2cb, and likely is not related to mef2ca homeotic function.