Differential elongation growth plays a key role in adaptation of plants to their environment. We are using apical hook, a structure formed by bending of the hypocotyl as a model to uncover the mechanisms underlying differential cell elongation in model plant Arabidopsis. We show that feedbacks between cell wall chemistry and chemical signals play a key role in hypocotyl bending during apical hook development. We demonstrate a mechanical asymmetry across the epidermal layer of the hypocotyl during apical hook development that correlates with asymmetric distribution of pectin methylesterification. Genetic approaches using inducible PME and PMEI expression demonstrate that perturbing this asymmetric pectin methylestrification leads to defects in apical hook development. Downtream, differential pectin methylestrification across the hook is required for generation of asymmetric auxin response and in t urn auxin distribution impacts pectin methylesterification. Finally pectin methylestrerification impacts not only auxin response but also polar auxin transport components as well. Importantly, our data indicates that pectin methylestrerification impacts not only auxin response but polar auxin transport components as well. Taken together, our results indicate how mechanical signals via cell wall chemistry modulate chemical signals such as plant hormone auxin and vice-versa to control differential cell elongation in plants.