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Fig. 5
tmem88a inhibition alters cardiac ventricular polarity. Following knockdown of tmem88a by ATG-targeting or splice-blocking morpholinos, conduction velocity as measured in isolated hearts following staining with Di-8-ANEPPS was significantly increased along the outer curvature of the ventricle (A). This difference is also illustrated through isochronal maps showing voltage propagation along a control heart (B) versus hearts from embryos injected with the ATG (C) or splice-blocking (D) morpholinos (isochrons are 5 mseconds apart, conduction goes from blue to red). There was no apparent change in connexin 43 expression or cell number accompanying this alteration in cell coupling. Expression of connexin 43 (E) was strong in the atria, but weak in the ventricles in control hearts (F), and did not appear to change with inhibition of tmem88a (ATG-blocking morpholino in G, splice-blocking morpholino in H). Cell number as measured by manual counting of ventricular nuclei (I) revealed no obvious differences between control hearts (J) and hearts from embryos injected with the ATG (K) or splice (L) morpholinos (β-catenin in green, DAPI in blue). *P<0.05 (Student’s t-test, n>4 for each condition). Error bars indicate standard error.