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Mechanobiology of Disease
Poster Abstracts
122
72-POS
Board 72
Basolateral Protrusion and Apical Contraction Cooperatively Drive Drosophila Germband
Elongation
Zijun Sun
1
, Murat Shagirov
1
, Yusuke Hara
1
, Christopher Amourda
1
, Timothy Saunders
1,2,3
,
Yusuke Toyama
1,2,4
.
1
Mechanobiology Institute, Singapore, Singapore,
2
Department of Biological Sciences, National
University of Singapore, Singapore, Singapore,
3
Institute for Molecular and Cell Biology,
Agency for Science Technology and Research, Singapore, Singapore,
4
Temasek Life Sciences
Laboratory, Singapore, Singapore.
Robust tissue morphological changes require an integration of cellular mechanics that evolve
over time and in three dimensional space. During animal axis elongation, cell intercalation is the
key mechanism for tissue convergent extension1, and it is known that the associated polarized
apical junction remodelling is driven by myosin-dependent contraction during Drosophila
germband extension2-4. However, the contribution of the basolateral cellular mechanics remains
poorly understood. Here, we characterize how cells coordinate their shape and movement from
the apical to the basal side during rosette pattern formation, a hallmark of cell intercalation. We
reveal that there are distinct apical and basolateral mechanisms required for intercalation. As
previously reported, the contraction of actomyosin cables formed in a subset of cells (the
anterior/posterior (A/P) cells) drives apical rosette formation4. In contrast, basolateral rosette
formation is driven by cells mostly located at the dorsal/ventral (D/V) part of the cluster (D/V
cells). These cells exhibit wedge-shaped basolateral protrusions and migrate towards each other
along the D/V axis. Surprisingly, we find that the formation of basolateral rosettes precedes that
of the apical rosettes. Impeding the apical acto-myosin contractility does not prevent the
resolution of rosettes on the basal side. This indicates that the establishment of basal rosettes is
independent of apical contractility. Instead, by selectively blocking Rac activity, we show that
Rac-dependent protrusive motility is required for basal rosette formation. Furthermore, by using
an RNAi screen we identify a component regulating basal rosette formation, the inhibition of
which leads to abnormal basal intercalation but retains apical rosette formation and eventually
results in delayed extension. Our data show that in addition to apical contraction, active cell
migration driven by basolateral protrusions plays a pivotal role in body axis elongation.