Further Development 9.3: It Takes Strength to Bend a Fly

The Genetics of Axis Specification in Drosophila

To move anything takes force, and understanding the mechanical forces involved in morphogenesis has recently become an area of great interest to developmental biologists. Drosophila gastrulation presents many questions relevant to these areas of study. For example, what are the biomechanics driving invagination of mesoderm at the ventral furrow?

First, realize that the cellularized blastoderm is an epithelium, so its cells have strong junctional attachments (adhesion) to one another. This tissue, therefore, should not break under strain, but it may change shape. It was recently discovered that just prior to mesoderm invagination, myosin becomes most active in the cells at the ventral midline of the embryo. (As you likely already know, myosin is a motor protein that associates with actin filaments to build subcellular contractile machines—think muscle cells.) Over time, this highly active myosin not only accumulates in the apex of cells at the midline, but also becomes organized into arrays along the cells’ anterior-to-posterior axis. This axial orientation of actomyosin arrays concentrated in ventral cells along the midline causes anisotropic tension (i.e., asymmetric, not uniform) directed along the length of the future furrow (Figure 1; Chanet et al. 2017; Heer et al. 2017). The oriented apical constriction of the midline ventral cells causes them to become wedge-shaped rather than conical, resulting in a furrow rather than a pit. This is just one example of how force plays a role in controlling cellular behavior that changes the shape of a tissue. Keep the momentum going and seek out additional processes that are under the regulation of biophysical parameters—the reality is, they all are.

Figure 1 Physical forces drive invagination of the ventral furrow. (A) The cellularized blastoderm will begin to activate higher levels of myosin in the cells at the ventral midline and preferentially at their apical surface (right, faint green labeling in fluorescent micrograph and in adjacent schematic). (B) Epithelial adhesions paired with differential activation of myosin and tissue geometry create mechanical constraints that affect the orientation of actomyosin meshworks. The A/P oriented arrays of myosin (yellow arrows; fluorescent micrograph) in the cells at the ventral midline generate tension along the anterior-posterior axis. (C) The combination of tissue geometry and tension of these anterior-to-posterior meshworks cause the tissue to fold inward at a right angle to the anterior-posterior axis, creating a long and narrow ventral furrow. (After N. C. Heer et al. 2017. Development 15: 1876–1886; S. Chanet et al. 2017. Nat Commun 8: 15014/CC BY 4.0.)


Chanet, S., C. J. Miller, E. D. Vaishnav, B. Ermentrout, L. A. Davidson and A. C. Martin. 2017. Actomyosin meshwork mechanosensing enables tissue shape to orient cell force. Nat. Commun. 8: 15014
PubMed Link

Heer, N. C., P. W. Miller, S. Chanet, N. Stoop, J. Dunkel and A. C. Martin. 2017. Actomyosin-based tissue folding requires a multicellular myosin gradient. Development 144: 1876–1886.
PubMed Link

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