Control of Cell Division Orientation by Cell-intrinsic and Tissue-scale Forces During Drosophila Axis Elongation

Abstract

Oriented cell division (OCD) within the plane of a tissue is a conserved mechanism of tissue elongation, maintenance and organization. Here, we investigate how myosin II polarity downstream of leucine-rich-repeat (LRR) receptors influence OCD in the early Drosophila embryo. Following convergent extension, cells in the ventral mesectoderm (VME) and cells along compartment boundaries in the lateral neuroectoderm (LNE) divide parallel to the anterior-posterior axis. We analyzed division angles in live mutant embryos lacking myosin polarity at specific cell-cell junctions and show that both cell-intrinsic polarity and non-autonomous outside forces influence division angles differently between the two tissues. We demonstrate that a minimum threshold of myosin polarity, not overall myosin levels, is required to bias divisions as the embryo elongates. In the LNE, we present evidence that strong myosin polarity mediated by Tartan at compartment boundaries biases boundary divisions while simultaneously buffering cells inside compartments from pulling by the posterior midgut. In the VME, our results suggest that signaling by Tartan and Toll family receptors (Toll-2, Toll-6, Toll-8) primes all cells to become responsive to posterior pulling to strongly bias cell divisions. Together, this study shows that cell-intrinsic LRR receptor signaling, primarily mediated by Tartan, interacts with cell-extrinsic pulling forces to shape the distinct patterns of OCD observed in the Drosophila germband.