Focal adhesion (FA) turnover depends on microtubules and actin. Microtubule ends are captured at FAs, where theyinduce rapid FAdisassembly. However,actin’srolesare less clear. Here, we usepolarization-resolved microscopy,FRAP, livecell imaging, anda mutant of Adenomatous polyposis coli(APC-m4) defective in actin nucleationtoinvestigatethe roleof actinassemblyin FA turnover. Weshow that APC-mediated actin assembly is criticalfor maintaining normalF-actinlevels,organization,and dynamics at FAs, along with organization of FA components. In wild type cells,microtubulesarecaptured repeatedlyat FAsasthey mature, butoncea FA reaches peak maturity,the next microtubule capture event leads todelivery of an autophagosome, triggering FA disassembly. InAPC-m4 cells,microtubule capture frequency and duration are altered, and there arelong delays between autophagosome delivery and FA disassembly. Thus, APC-mediated actin assemblyis required for normalfeedback between microtubules and FAs, and maintainingFAsin astate‘primed’ for microtubule-induced turnover.