Graham Anderson, Lendert Gelens, Julie Baker, and Jim Ferrell featured on the cover of Cell Reports

Graham Anderson, Lendert Gelens, Julie Baker, and Jim Ferrell featured on the cover of Cell Reports

The October 3 2017 issue of Cell Reports features a research paper, “Desynchronizing Embryonic Cell Division Waves Reveals the Robustness of Xenopus laevis Development,” from Jim Ferrell’s and Julie Baker’s labs, with Graham Anderson and Lendert Gelens as co-first authors. Graham’s and Lendert’s work started with an old observation: when Xenopus embryos cleave, first in two, then in four, and so on, the cell divisions happen almost, but not quite, synchronously. If you look carefully you can see that there is actually a wave of cell division that sweeps from one side of the embryo to the other. It looks to the eye a lot like a contraction wave passing through the human heart. Graham and Lendert set out to see whether the wave of cell divisions is due to some sort of coupling between the cells. It turns out it is not; different cells in the embryo have their cell cycle oscillators running at different speeds, and each cell completely ignores the rhythm of it neighbors’ cell cycles. They then went on to show if they artificially desynchronized the normal wave of cell divisions, some of the early steps of development would be highly abnormal, but, miraculously, the embryos would correct these abnormalities later in development and turn into normal tadpoles. This finding underscores the robustness of the process of embryonic development.

To read the original Cell Reports cover article, please click here.

A summary of the paper is included below:

The early Xenopus laevis embryo is replete with dynamic spatial waves. One such wave, the cell division wave, emerges from the collective cell division timing of first tens and later hundreds of cells throughout the embryo. Here, we show that cell division waves do not propagate between neighboring cells and do not rely on cell-to-cell coupling to maintain their division timing. Instead, intrinsic variation in division period autonomously and gradually builds these striking patterns of cell division. Disrupting this pattern of division by placing embryos in a temperature gradient resulted in highly asynchronous entry to the midblastula transition and misexpression of the mesodermal marker Xbra. Remarkably, this gene expression defect is corrected during involution, resulting in delayed yet normal Xbra expression and viable embryos. This implies the existence of a previously unknown mechanism for normalizing mesodermal gene expression during involution.

Congratulations to Graham Anderson, Lendert Gelens, and Dr. Ferrell!