Figure 3.—

The gat1∆ mutant is unable to utilize a wide variety of nitrogen sources. Tenfold spot dilution assays of wild-type H99 and GATA-type deletion mutants for nitrogen utilization showed that the gat1∆ mutant is unable to grow on YNB supplemented with 10 mm ammonium, uric acid, urea, or creatinine but exhibits only a slight growth defect compared to wild type on 10 mm proline. Complementation of the gat1∆ mutant with the GAT1 gene restored wild-type nitrogen utilization phenotype (Figure S3).