Abstract
Wnt signaling plays a critical role in craniofacial patterning, as well as tooth and bone development.
Rspo2
and
Rspo3
are key regulators of Wnt signaling. However, their coordinated function and relative requirement in craniofacial development and odontogensis are poorly understood. We showed that in zebrafish
rspo2
and
rspo3
are both expressed in osteoprogenitors in the embryonic craniofacial skeleton. This is in contrast to mouse development, where
Rspo3
is expressed in osteoprogenitors while
Rspo2
expression is not observed. In zebrafish,
rspo2
and
rspo3
are broadly expressed in the pulp, odontoblasts and epithelial crypts. However, in the developing molars of the mouse,
Rspo3
is largely expressed in the dental follicle and alveolar mesenchyme while
Rspo2
expression is restricted to the tooth germ. While
Rspo3
ablation in the mouse is embryonic lethal, zebrafish
rspo3
-/- mutants are viable with modest decrease in Meckel’s cartilage rostral length. However, compound disruption of
rspo3
and
rspo2
revealed synergistic roles of these genes in cartilage morphogenesis, fin development, and pharyngeal tooth development. Adult
rspo3
−/−
zebrafish mutants exhibit a dysmorphic cranial skeleton and decreased average tooth number. This study highlights the differential functions of
Rspo2
and
Rspo3
in dentocranial morphogenesis in zebrafish and in mouse.