Lateral root (LR) formation in Arabidopsis is regulated by auxin signaling through AUXIN RESPONSE FACTOR transcriptional activators, ARF7 and ARF19, and auxin/indole-3-acetic acid (Aux/IAA) repressors, including SOLITARY-ROOT (SLR)/IAA14. Previous studies have strongly suggested that, in the gain-of-function slr-1 mutant, stabilized mutant IAA14 (mIAA14) protein inactivates ARF7/19 functions, thereby completely blocking LR initiation. However, the mechanism of inactivation is still unknown. We have now identified an extragenic suppressor mutation of slr-1, suppressor of slr2 (ssl2), which specifically restores LR formation in the slr-1 mutant, and have found that SSL2 negatively regulates the auxin-induced pericycle cell divisions required for LR initiation. The SSL2 gene encodes PICKLE (PKL), a homologue of the animal chromatin-remodeling factor CHD3/Mi-2, and LR formation restored in pkl/ssl2 slr-1 mutants depends on ARF7/19 functions, suggesting that ARF7/19-dependent transcription takes place if there is a pkl/ssl2 mutation in slr-1. In animals, Mi-2 represses transcription as a subunit of the NuRD/Mi-2 complex containing histone deacetylases (HDACs). Inhibition of HDAC activity by trichostatin A also results in LR formation in the slr-1 mutant, but not in the slr-1 arf7 arf19 triple mutant, suggesting that normal HDAC activity is required for the mIAA14-mediated inactivation of ARF7/19 functions in LR initiation. Taken together, our data suggest that PKL/SSL2-mediated chromatin remodeling negatively regulates auxin-mediated LR formation in Arabidopsis.