The myosin ID pathway and left–right asymmetry in Drosophila

Abstract

Summary: Drosophila is a classical model to study body patterning, however left-right (L/R) asymmetry had remained unexplored, until recently. The discovery of the conserved myosin ID gene as a major determinant of L/R asymmetry has revealed a novel L/R pathway involving the actin cytoskeleton and the adherens junction. In this process, the HOX gene Abdominal-B plays a major role through the control of myosin ID expression and therefore symmetry breaking. In this review, we present organs and markers showing L/R asymmetry in Drosophila and discuss our current understanding of the underlying molecular genetic mechanisms. Drosophila represents a valuable model system revealing novel strategies to establish L/R asymmetry in invertebrates and providing an evolutionary perspective to the problem of laterality in bilateria. genesis 52:471-480,

When and Why Did Brains Break Symmetry?

“…In fact, it could well be that Nodal is an ancestral mechanism for the development of left/right asymmetry in several organs or tissues [42]. Research on the genes involved in symmetry and breaking symmetry in invertebrates is in its infancy, but, although is still debated, other genes (e.g., the Hox gene [45]) have emerged as potentially similar determinants of gut asymmetry in invertebrates and vertebrates [46]. Whether the same or similar genes are involved in the genesis of neural asymmetry remains to be investigated, and the nematode, C. elegans, and the zebrafish are proving to be useful models for this research [47,48].…”

Cytoskeletal Symmetry Breaking and Chirality: From Reconstituted Systems to Animal Development

“…The breakthrough discovery that fueled L/R patterning research was the identification of unconventional myosin ID (myoID/myo31DF) mutants. These show an inversion of the L/R axis and reversal of all L/R asymmetric organs, e.g., gut looping, spermiduct coiling, rotation of the male terminalia [206][207][208]. MyoID belongs to the class I non-filamentous myosins, which are actin-binding motor proteins known for roles in actin cytoskeleton organization, cell motility, and endocytosis [209].…”

“…Surprisingly, its loss does not lead to reversion of L/R asymmetries like the loss of myoID, rather, L/R asymmetry is lost. Noselli and colleagues have argued that this reveals the existence of a sinistral activity since inversion is only apparent in a myoID mutant context [208].…”

The Atypical Cadherin Dachsous Controls Left-Right Asymmetry in Drosophila

“…In contrast to vertebrates, Drosophila LR markers are relatively simple and homogeneous as they are restrained to tubular organs that undergo dextral morphogenesis; these include male terminalia rotation, looping of the larval and adult gut, and testis (Hozumi et al, 2006;Gé minard et al, 2014;Spé der et al, 2006;Coutelis et al, 2008). Genes controlling LR asymmetry in flies have only recently been identified.…”

“…Genes controlling LR asymmetry in flies have only recently been identified. The conserved type ID myosin gene (myosin ID, myoID; also known as myo31DF) (Mooseker and Cheney, 1995;Morgan et al, 1995) is unique, as myoID loss of function leads to complete situs inversus with all asymmetric organs developing as sinistral (Hozumi et al, 2006;Gé minard et al, 2014;Spé der et al, 2006;Coutelis et al, 2008). The expression of myoID-and, hence, LR symmetry breaking-is under the direct control of the HOX transcription factor Abdominal-B (Coutelis et al, 2013).…”