Abstract
C(4) photosynthesis in grasses relies on a specialized leaf anatomy. In maize, this "Kranz" leaf anatomy is patterned in part by the duplicated SCARECROW (SCR) genes ZmSCR1 and ZmSCR1h. Here we show that in addition to patterning defects, chlorophyll content and levels of transcripts encoding Golden2-like regulators of chloroplast development are significantly lower in Zmscr1; Zmscr1h mutants than in wild-type. These perturbations are not associated with changes in chloroplast number, size, or ultrastructure. However, the maximum rates of carboxylation by ribulose bisphosphate carboxylase/oxygenase (RuBisCO, V (cmax)) and phosphoenolpyruvate carboxylase (PEPC, V (pmax)) are both reduced, leading to perturbed plant growth. The CO(2) compensation point and (13)C‰ of Zmscr1;Zmscr1h plants are both normal, indicating that a canonical C(4) cycle is operating, albeit at reduced overall capacity. Taken together, our results reveal that the maize SCR genes, either directly or indirectly, play a role in photosynthetic development. SIGNIFICANCE STATEMENT: SCARECROW (SCR) is one of the best studied plant developmental regulators, however, its role in downstream plant physiology is less well-understood. Here, we have demonstrated that SCR is required to establish and/or maintain photosynthetic capacity in maize leaves.