With the rise of new tools, from controlled genetic manipulations and optogenetics to improved microscopy, it is now possible to make clear, quantitative and reproducible measurements of biological processes. The humble fruit fly Drosophila melanogaster, with its ease of genetic manipulation combined with excellent imaging accessibility, has become a major model system for performing quantitative in vivo measurements. Such measurements are driving a new wave of interest from physicists and engineers, who are developing a range of testable dynamic models of active systems to understand fundamental biological processes. The reproducibility of the early Drosophila embryo has been crucial for understanding how biological systems are robust to unavoidable noise during development. Insights from quantitative in vivo experiments in the Drosophila embryo are having an impact on our understanding of critical biological processes, such as how cells make decisions and how complex tissue shape emerges. Here, to highlight the power of using Drosophila embryogenesis for quantitative biology, I focus on three main areas: (1) formation and robustness of morphogen gradients; (2) how gene regulatory networks ensure precise boundary formation; and (3) how mechanical interactions drive packing and tissue folding. I further discuss how such data has driven advances in modelling.
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http://dx.doi.org/10.1016/j.cdev.2021.203722 | DOI Listing |
J Cell Biol
April 2025
Department of Physics and Astronomy, University of Denver, Denver, CO, USA.
In the early Drosophila embryo, germband elongation is driven by oriented cell intercalation through t1 transitions, where vertical (dorsal-ventral aligned) interfaces contract and then resolve into new horizontal (anterior-posterior aligned) interfaces. Here, we show that contractile events produce a continuous "rectification" of cell interfaces, in which interfaces systematically rotate toward more vertical orientations. As interfaces rotate, their behavior transitions from elongating to contractile regimes, indicating that the planar polarized identities of cell-cell interfaces are continuously re-interpreted in time depending on their orientation angle.
View Article and Find Full Text PDFEmbryogenesis is remarkably robust to temperature variability, yet there is limited understanding of the homeostatic mechanisms that offset thermal effects during early development. Here, we measured the thermal acclimation response of upper thermal limits and profiled chromatin state and the transcriptome of embryos (Bownes Stage 11) using single-nuclei multiome ATAC and RNA sequencing. We report that thermal acclimation, while preserving a common set of primordial cell types, rapidly shifted the upper thermal limit.
View Article and Find Full Text PDFbioRxiv
January 2025
Department of Molecular Biology, Princeton University, Princeton 08544.
A lack of tools for detecting receptor activity has limited our ability to fully explore receptor-level control of developmental patterning. Here, we extend a new class of biosensors for receptor tyrosine kinase (RTK) activity, the pYtag system, to visualize endogenous RTK activity in . We build biosensors for three RTKs that function across developmental stages and tissues.
View Article and Find Full Text PDFare endosymbiotic bacteria inducing various reproductive manipulations of which cytoplasmic incompatibility (CI) is the most common. CI leads to reduced embryo viability in crosses between males carrying and uninfected females or those carrying an incompatible symbiont strain. In the mosquito , the Pip causes highly complex crossing patterns.
View Article and Find Full Text PDFDev Cell
January 2025
Department of Cell and Systems Biology, University of Toronto, Toronto, ON M5S 3G5, Canada; Ted Rogers Centre for Heart Research, University of Toronto, Toronto, ON M5G 1M1, Canada; Institute of Biomedical Engineering, University of Toronto, Toronto, ON M5S 3G9, Canada; Developmental and Stem Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 1X8, Canada. Electronic address:
Embryonic wounds repair rapidly, with no inflammation or scarring. Embryonic wound healing is driven by collective cell movements facilitated by the increase in the volume of the cells adjacent to the wound. The mechanistic target of rapamycin (mTor) complex 1 (TORC1) is associated with cell growth.
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