Involved in the control of cell movement by regulating actin cytoskeleton homeostasis and filopodium and lamellipodium formation. Associates with the membrane via the insertion of the N-terminal N-myristoyl chain and the partial insertion of the effector domain. Strongly expressed in brain and eye. Also detected at lower levels in muscle. Detected from 24 to 72 hours post-fertilization (hpf). Morpholino knockdown of the protein results in reduced head and eye size, a ventrally curved body, and enlarged brain vesicles. In the craniofacial cartilage, the ceratobranchial arches are reduced. Formation of ceratohyal cartilage is disrupted with an abnormal angle relative to wild-type. Morphogenesis of the developing neural tube is abnormal, with a smaller angle between the walls of the hindbrain neuroepithelium at 24 hours post-fertilization (hpf) and in some cases a partial opening in the dorsal region. Some deformation of the midbrain walls is also found. Retinal development is significantly delayed; no retinal ganglion cells (RGCs) are detected at 30 hpf and reduced numbers are found at 60 hpf. RGCs also appear to be mislocalized. In about a third of embryos, three instead of two otoliths are detected in the inner ear. Cilium length in Kupffer's vesicle is significantly reduced. Cilia in the olfactory placode also appear to be fewer in number and have reduced length. Double morpholino knockdown of marcksl1a and marckls1b results in a more pronounced developmental delay in the retina. Double morpholino knockdown of marcksb and marcksl1b results in retinal morphogenesis defects of increased severity. The optic cup structure is not apparent, and very few atoh7-positive retinal ganglion cell precursors are detected. Double morpholino knockdown of marcksb and marcksl1b also results in more severe defects in neural tube morphology, with partial duplications of the neural tube in the hindbrain region. Belongs to the MARCKS family.