Plants can exploit complex suites of biochemical, morphological, and physiological mechanisms to defend against herbivory. This research expands that body of knowledge by investigating mechanisms of defense in maize (Zea mays) against one of its most economically important pests, the western corn rootworm (Diabrotica virgifera virgifera, WCR). Natural variation for resistance and tolerance to WCR larval herbivory has been previously reported; however, characterization of the underlying genetic architecture has remained elusive. The results from three separate studies are presented that confirm heritable variation exists for WCR resistance that is both experimentally tractable and reproducible. The findings highlight that both genetic and environmental components contribute to the observed variation and interactions exist between rootworm population dynamics and root phenology. Using F2, BC1, and DH populations capturing natural variation for three native resistance traits, we demonstrate that discrete regions on chromosomes 2, 3, 5, and 7 are consistently associated with a resistance phenotype. QTL co-localized across analysis populations that were evaluated in different locations and years. Among 21 QTL fixed in the DH population, between 46% and 56% of the variation was explained for three resistance traits. The alleles were found to act robustly by reducing node-injury and increasing root biomass, which was confirmed in hybrid testcrosses. In a separate study, we identified particular physiological and genetic mechanisms of response to WCR root herbivory and revealed evidence of genetic overcompensation. A QTL on c3 (bin 3.05) was localized to a 2.8 cM region and was associated with increased growth rate under high herbivory. The sps2 gene involved in regulating source-sink transition fell precisely within the QTL interval, and is a possible candidate in the herbivory stress response. These results advance our current understanding of host-plant defense and also provide a route for applied maize improvement by providing a genetic framework for native resistance that can be exploited to reduce larval feeding damage by WCRs.