The pharynx muscular pump comprises 20 muscle cells which are gap junction coupled, and possess orthologues of the human voltage-dependent Ca2+ channel Cav1.2 (i.e. EGL-19), the SR-Ca2+ storage protein CASQ2 (i.e. CSQ-1) and the ryanodine receptor (RyR; UNC-68). The similar physiology, pumping frequencies, and shape of the action potential imply the pharynx as a potential model for the human heart, possibly allowing to study mechanisms of arrhythmia like catecholaminergic polymorphic ventricular tachycardia (CPVT) or Timothy Syndrome (LQT8). Pharyngeal pumping was recorded by electropharyngeograms (EPGs) in
unc-68 and
csq-1 deletions, or in
egl-19 point mutants, as well as in pharmacologically treated animals. By engineering animals carrying CPVT related mutations of the RyR (e.g. R4743C) or
csq-1 as well as using
egl-19 alleles resembling mutants implicated in LQT8, we analyze in detail whether arrhythmic pumping can be provoked. Even though the RyR is not required for basal pumping, activation of RyRs by caffeine increased the pumping frequency. The RyR point mutant R4743C could rescue
unc-68 (
r1162) mutants, based on swimming assays, indicative for a functional rescue in body wall muscles. As spontaneous pumping is not regular enough to analyze arrhythmia faithfully, we use the light-activated cation channels Channelrhodopsin-2 (ChR2) or its color-shifted variant C1V1, expressed in pharyngeal muscle, to depolarize the plasma membrane, evoke muscle contraction, and to "pace" the pharynx at up to 4 Hz. For the UNC-68(R4743C) mutant, we observed an increase in irregular pump events, and we will perform similar analyses of
egl-19 and of engineered CPVT-related
csq-1 mutants. We will further analyze these mutants by Ca2+ imaging with the red-fluorescent Ca2+ indicator RCaMP, which, as we could show, can faithfully report Ca2+ dynamics in the pharynx.