One of the striking examples of robust developmental patterning is the rhythmic segmentation of somites, which are precursors of the vertebral column. Somitogenesis is controlled by the interaction of a gene expression oscillator (the segmentation clock) and posteriorly-moving signaling gradients (the wavefront). The clock provides the temporal information (periodicity), while the signaling gradients provide the spatial information (position of segment boundaries). Pattern formation is regulative; embryos robustly form a fixed number of patterns and the sizes of patterns scale with body or tissue sizes even when total cell number, cell sizes or growth rate are changed experimentally. In order to elucidate the mechanism conferring spatial precision, we have combined surgical and pharmacological experiments with reaction-diffusion based multicellular mathematical modeling. We have shown that a spatial signal differentiator circuit controls segmental determination and pattern scaling. We have found that neighboring cells compare their signal activity to accurately interpret positional information along tissue and commit for segmentation and differentiation. In order to elucidate the mechanism conferring temporal precision, we have counted transcripts of the segmentation clock genes in single cells by performing single-molecule fluorescent in situ hybridization experiments and analyzed the data with our statistical model. We have shown that clock genes have low RNA amplitudes, expression variability is driven by transcriptional bursts due to gene extrinsic sources. We have further shown that Notch signaling suppresses expression variability and synchronizes segmentation clock oscillations by augmenting transcription burst frequencies and limiting gene extrinsic noise. These findings illustrate potential mechanisms of pattern scaling in other developing tissues and inspire engineering robust tissue patterns.