Substrate-recognition component of a DCX (DDB1-CUL4-X-box) E3 ubiquitin-protein ligase complex involved in cell cycle control and autophagy (PubMed:23348054). The DCX(AMBRA1) complex specifically mediates the polyubiquitination of target proteins (By similarity). Acts as an upstream master regulator of the transition from G1 to S cell phase: ambra1a specifically recognizes and binds phosphorylated cyclin-D (ccnd1, ccnd2 and ccnd3), leading to cyclin-D ubiquitination by the DCX(AMBRA1) complex and subsequent degradation (By similarity). Acts as a regulator of Cul5-RING (CRL5) E3 ubiquitin-protein ligase complexes by mediating ubiquitination and degradation of Elongin-C (eloc) component of CRL5 complexes (By similarity). Acts as a key regulator of autophagy by modulating the BECN1-PIK3C3 complex: controls protein turnover during neuronal development, and regulates normal cell survival and proliferation (By similarity). In normal conditions, ambra1a is tethered to the cytoskeleton via interaction with dyneins light chains (By similarity). Upon autophagy induction, ambra1a is released from the cytoskeletal docking site to induce autophagosome nucleation by mediating ubiquitination of proteins involved in autophagy (By similarity). Also acts as an activator of mitophagy (By similarity). Required for skeletal muscle development (PubMed:24922546). Protein modification; protein ubiquitination. Component of the DCX(AMBRA1) E3 ubiquitin ligase complex. Localizes to the cytoskeleton in absence of autophagy induction. Upon autophagy induction, ambra1a relocalizes to the endoplasmic reticulum to enable autophagosome nucleation. Partially localizes at mitochondria in normal conditions. Expressed both maternally and zygotically. Present as maternal transcripts in the eggs and display a gradual decline until 8 hours post-fertilization (hpf), being replaced by zygotic mRNAs from 12 hpf onwards (PubMed:23348054). After 24 hpf, the transcripts are mainly localized in the brain and otic vesicles (PubMed:23348054). Morpholino knockdown of ambra1a causes impaired dorso-ventral patterning in embryos (PubMed:23348054). Morpholino knockdown of ambra1a and ambra1b results in reduced autophagy and increased apoptosis during embryogenesis (PubMed:23348054). Morpholino knockdown of ambra1a and ambra1b results in impaired locomotion, caused by abnormal myogenesis (PubMed:24922546). Belongs to the WD repeat AMBRA1 family.