Myosin II is not required for Drosophila tracheal branch elongation and cell intercalation

Abstract

The Drosophila tracheal system consists of an interconnected network of monolayered epithelial tubes that ensures oxygen transport in the larval and adult body. During tracheal dorsal branch (DB) development, individual DBs elongate as a cluster of cells, led by tip cells at the front and trailing cells in the rear. Branch elongation is accompanied by extensive cell intercalation and cell lengthening of the trailing stalk cells. Although cell intercalation is governed by Myosin II (MyoII)-dependent forces during tissue elongation in the Drosophila embryo that lead to germ-band extension, it remained unclear whether MyoII plays a similar active role during tracheal branch elongation and intercalation. Here, we have used a nanobody-based approach to selectively knock down MyoII in tracheal cells. Our data show that, despite the depletion of MyoII function, tip cell migration and stalk cell intercalation (SCI) proceed at a normal rate. This confirms a model in which DB elongation and SCI in the trachea occur as a consequence of tip cell migration, which produces the necessary forces for the branching process. ABSTRACTThe Drosophila tracheal system consists of an interconnected network of monolayered epithelial tubes that ensures oxygen transport in the larval and adult body. During tracheal dorsal branch (DB) development, individual DBs elongate as a cluster of cells, led by tip cells at the front and trailing cells in the rear. Branch elongation is accompanied by extensive cell intercalation and cell lengthening of the trailing stalk cells. Although cell intercalation is governed by Myosin II (MyoII)-dependent forces during tissue elongation in the Drosophila embryo that lead to germ-band extension, it remained unclear whether MyoII plays a similar active role during tracheal branch elongation and intercalation. Here, we have used a nanobodybased approach to selectively knock down MyoII in tracheal cells. Our data show that, despite the depletion of MyoII function, tip cell migration and stalk cell intercalation (SCI) proceed at a normal rate. This confirms a model in which DB elongation and SCI in the trachea occur as a consequence of tip cell migration, which produces the necessary forces for the branching process.

Endothelial cell rearrangements during vascular patterning require PI3-kinase-mediated inhibition of actomyosin contractility

“…Together, this supports the notion that actomyosin activity has to be low for cell rearrangements to occur. This is not unique of endothelial cells as it has also been observed in Drosophila epithelial tracheal tubes and in tumour cells 49 , 50 . Upon contraction, the actomyosin machinery transmits force to cell−cell contacts and regulates junctional remodelling 12 , 50 .…”

Applying Antibodies Inside Cells: Principles and Recent Advances in Neurobiology, Virology and Oncology

“…This approach is especially attractive for model organisms with GFP-tagged proteins, such as those often used in developmental biology. In zebrafish and flies, this approach has already been successfully applied [ 124 – 126 ]. Various tags and motifs can be employed to target antibodies and their antigens for degradation, such as providing the binder with an AiD, a proline, aspartate or glutamate, serine and threonine (PEST) motif, the Von Hippel Lindau protein, Speckle-type POZ protein (SPOP), an F-box domain or the catalytic domain of a ubiquitin ligase [ 6 , 124 , 127 – 132 ].…”

The devil is in the mesoscale: Mechanical and behavioural heterogeneity in collective cell movement

“…A commonly studied example is cells at the edge or front of a group seemingly 'leading' migration [16]. In some cases, such as tracheal branching [17,18] and sprouting angiogenesis [19], leader cells actively migrate while follower cells undergo passive intercalation or proliferation; in other cases, such as neural crest migration [20], all cells undergo active migration, but leader cells may guide directionality or interact with the microenvironment differently from the rest of the group, e.g. reacting to chemotactic signals [21,22] or possibly by modifying the extracellular matrix.…”