Biophysical Society Thematic Meeting | Singapore

Mechanobiology of Disease

Poster Abstracts

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.

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