We study systems of identical coupled oscillators introducing a distribution of delay times in the coupling. For arbitrary network topologies, we show that the frequency and stability of the fully synchronized states depend only on the mean of the de
lay distribution. However, synchronization dynamics is sensitive to the shape of the distribution. In the presence of coupling delays, the synchronization rate can be maximal for a specific value of the coupling strength.
We study the effects of delayed coupling on timing and pattern formation in spatially extended systems of dynamic oscillators. Starting from a discrete lattice of coupled oscillators, we derive a generic continuum theory for collective modes of long
wavelength. We use this approach to study spatial phase profiles of cellular oscillators in the segmentation clock, a dynamic patterning system of vertebrate embryos. Collective wave patterns result from the interplay of coupling delays and moving boundary conditions. We show that the phase profiles of collective modes depend on coupling delays.
Coupled biological oscillators can tick with the same period. How this collective period is established is a key question in understanding biological clocks. We explore this question in the segmentation clock, a population of coupled cellular oscilla
tors in the vertebrate embryo that sets the rhythm of somitogenesis, the morphological segmentation of the body axis. The oscillating cells of the zebrafish segmentation clock are thought to possess noisy autonomous periods, which are synchronized by intercellular coupling through the Delta-Notch pathway. Here we ask whether Delta-Notch coupling additionally influences the collective period of the segmentation clock. Using multiple-embryo time-lapse microscopy, we show that disruption of Delta-Notch intercellular coupling increases the period of zebrafish somitogenesis. Embryonic segment length and the spatial wavelength of oscillating gene expression also increase correspondingly, indicating an increase in the segmentation clocks period. Using a theory based on phase oscillators in which the collective period self-organizes because of time delays in coupling, we estimate the cell-autonomous period, the coupling strength, and the coupling delay from our data. Further supporting the role of coupling delays in the clock, we predict and experimentally confirm an instability resulting from decreased coupling delay time. Synchronization of cells by Delta-Notch coupling regulates the collective period of the segmentation clock. Our identification of the first segmentation clock period mutants is a critical step toward a molecular understanding of temporal control in this system. We propose that collective control of period via delayed coupling may be a general feature of biological clocks.
Rhythmic and sequential subdivision of the elongating vertebrate embryonic body axis into morphological somites is controlled by an oscillating multicellular genetic network termed the segmentation clock. This clock operates in the presomitic mesoder
m (PSM), generating dynamic stripe patterns of oscillatory gene-expression across the field of PSM cells. How these spatial patterns, the clocks collective period, and the underlying cellular-level interactions are related is not understood. A theory encompassing temporal and spatial domains of local and collective aspects of the system is essential to tackle these questions. Our delayed coupling theory achieves this by representing the PSM as an array of phase oscillators, combining four key elements: a frequency profile of oscillators slowing across the PSM; coupling between neighboring oscillators; delay in coupling; and a moving boundary describing embryonic axis elongation. This theory predicts that the segmentation clocks collective period depends on delayed coupling. We derive an expression for pattern wavelength across the PSM and show how this can be used to fit dynamic wildtype gene-expression patterns, revealing the quantitative values of parameters controlling spatial and temporal organization of the oscillators in the system. Our theory can be used to analyze experimental perturbations, thereby identifying roles of genes involved in segmentation.
We study general aspects of active motion with fluctuations in the speed and the direction of motion in two dimensions. We consider the case in which fluctuations in the speed are not correlated to fluctuations in the direction of motion, and assume
that both processes can be described by independent characteristic time-scales. We show the occurrence of a complex transient that can exhibit a series of alternating regimes of motion, for two different angular dynamics which correspond to persistent and directed random walks. We also show additive corrections to the diffusion coefficient. The characteristic time-scales are also exposed in the velocity autocorrelation, which is a sum of exponential forms.
