Robustness is the invariant development of phenotypes against environmental changes and stochasticity. Mechanisms of robustness, however, are understudied. The Arabidopsis flower robustly develops four sepals of constant size and position, enclosing and protecting the reproductive organs before opening. Flowers of the development related myb-like1 (drmy1) mutant develop 3-5 sepals of variable sizes and positions, leaving gaps that compromise protection. The mutant phenotype correlates with disrupted auxin and cytokinin patterns, but it was unknown how DRMY1 controls robust hormone patterning and thus sepal development. Here, I showed that drmy1 has TOR signaling defects which reduce ribosomal content and translation. Reduced translation cannot maintain the protein level of ARABIDOPSIS RESPONSE REGULATOR7 (ARR7) and ARABIDOPSIS HISTIDINE PHOSPHOTRANSFER PROTEIN6 (AHP6), whose rapid synthesis is required to dampen cytokinin signaling. Elevated cytokinin signaling disrupts robust auxin patterning, leaving sporadic auxin patches in the meristem. In wild type, auxin maxima are robustly positioned in the four incipient sepal primordia. These auxin maxima restrict the expression of CUP-SHAPED COTYLEDON1 (CUC1) to adjacent regions, where CUC1 amplifies these maxima and promotes rapid sepal initiation. In drmy1 where robust auxin maxima are lost, CUC1 expression expands and overlaps with the sporadic auxin patches, stabilizing them to form incorrectly positioned auxin maxima and sepals. Thus, CUC1 promotes rapid sepal initiation but compromises robustness when hormone patterning is disrupted. Moreover, reducing tissue growth rate in drmy1 restores robust sepal initiation, further supporting such a tradeoff between morphogenesis speed and robustness. Lastly, I explored stochasticity in auxin signaling. I found that auxin-responsive gene expression is intrinsically stochastic in early-stage WT floral meristems, which canalizes into four incipient sepal primordia prior to sepal initiation. In summary, my work revealed a novel mechanism of developmental robustness, where DRMY1 supports rapid translation of key hormone signaling proteins, maintaining robust patterns of hormone signaling and gene expression that together promote robust organogenesis. My results show how disruptions in ubiquitous cellular processes, such as translation, do not cause a general growth reduction but have tissue-specific developmental consequences. Finally, my work shows how a single gene mediates the tradeoff between speed and robustness, two conflicting sides of morphogenesis.