Unconventional myosin that functions as actin-based motor protein with ATPase activity (PubMed:30467170). Binds to membranes enriched in phosphatidylinositol 4-5-bisphosphate, and can glide along actin filaments when anchored to a lipid bilayer (PubMed:30467170). Functions as antagonist for Myo31DF, an unconventional myosin with an essential role in the establishment of body left-right asymmetry (PubMed:16598258, PubMed:18521948, PubMed:22491943, PubMed:25659376, PubMed:30467170). Binds F-actin. Protein shifts from the basolateral to apical domain in enterocytes and follicle cells (PubMed:7589814). Colocalizes with the actin cytoskeleton (PubMed:22491943, PubMed:25659376). In the embryo, expressed in gastric caeca, midgut cells of the proventriculus, and in the mid and hindgut. In the larval and adult gut brush border, expressed in the microvilli. Also expressed at high levels in follicle cells during oogenesis. Expression starts at 8-12 hours embryonic development, continues to increase until third larval instar, disappears in pupae and is present at a low level in adults. Expression in embryogenesis is correlated with the formation of a brush border within the alimentary canal. In third instar larvae, detected in segment A8 of the male genital disk (PubMed:22491943). First detected at stage 12 in the embryonic anterior and posterior midgut, and in the stomatogastric nervous system. Detected in trachea at stage 14. Widely expressed in stage 16 in embryos (PubMed:25659376). The myosin motor domain contains the derminants for the direction of left-right body asymmetry. Viable and fertile, but adults have a shortened lifespan. Flies deficient in both Myo31DF and Myo61F are viable and fertile, but adults have a shorter lifespan than single mutants. Flies deficient in Myo61F show normal left-right asymmetry of the embryonic gut and normal, dextral rotation of male genitalia, and the same is observed in mutants deficient in both Myo61F and Myo95E. Mutants deficient in Myo31DF and Myo61F display stronger sinistral rotation of the male genitalia than mutants deficient for Myo31DF (PubMed:25659376). RNAi-mediated knockdown causes defects in embryonic midgut laterality, but only with low-frequency (PubMed:16598258). RNAi-mediated knockdown has no effect on normal, dextral rotation of male genitalia (PubMed:22491943). Combined RNAi-mediated knockdown of Myo31DF and Myo61F gives rise to the same phenotype as knockdown of Myo31DF alone, i.e sinistral rotation of the male genitalia (PubMed:22491943). Overexpression in larval epidermis causes sinistral twisting of the whole larval body. Ectopic expression in tracheal precursor cells causes sinistral spiraling of tracheal branches, giving rise to a spiraling ribbon shape instead of the normal smooth tube. Ectopic expression in epithelial cells causes increased elongation and a clear shift of the membrane orientation toward one side, so that the membrane is no longer perpendicular to the anterior-posterior axis (PubMed:30467170). Overexpression causes reversal of the normal left-right laterality of the embryonic midgut and hindgut (PubMed:16598258, PubMed:18521948). Overexpression causes loss of the normal dextral rotation of the male genitalia, and leads to sinistral rotation in some cases (PubMed:22491943). Belongs to the TRAFAC class myosin-kinesin ATPase superfamily. Myosin family.