Excess FasII impairs synaptic homeostasis.

Abstract

<p><b>(A-E)</b> Values for mEPSP amplitude (gray) and quantal content (QC; white) normalized to genetic controls (dashed line) that lack a homeostatic challenge (non-<i>GluRIII KD</i> or non-<i>GluRIIA</i> controls). <b>(A)</b> Trans-synaptic FasII overexpression (O/E) from the FasII endogenous locus (<i>FasII</i>^{<i>EP1462</i>}) shows partial impairment of synaptic homeostasis, as does <b>(B)</b> muscle-specific overexpression with <i>FasII</i>^{<i>EP1462</i>}. <b>(C)</b> Overexpressing specific isoforms of FasII does not impair homeostatic compensation. <b>(D)</b> Overexpressing Csk-YFP in addition to FasII^EP1462 fails to suppress the homeostatic defects of FasII O/E seen in B. <b>(E)</b> Neither <i>FasII</i> loss-of-function mutations nor <i>FasII</i> knockdown (KD) impairs synaptic homeostasis. <b>(F)</b> Average values for synaptic FasII and Dlg fluorescence intensity normalized to synapse area. <b>(G-H)</b> Representative images of FasII immunostaining for trans-synaptic FasII overexpression. Scale bar = 10 μm. * <i>p</i> < 0.05, ** <i>p</i> < 0.01, *** <i>p</i> < 0.001, ns—not significant (<i>p</i> > 0.08) by Student’s T-test comparing homeostatically challenged mutants to their unchallenged (non-<i>GluRIIA</i>) controls.</p