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PICKLE is required for SOLITARY‐ROOT/IAA14‐mediated repression of ARF7 and ARF19 activity during Arabidopsis lateral root initiation

2006; Wiley; Volume: 48; Issue: 3 Linguagem: Inglês

10.1111/j.1365-313x.2006.02882.x

1365-313X

Hidehiro Fukaki, Naohide Taniguchi, Masao Tasaka,

Plant Gene Expression Analysis

Summary 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.