The epigenetic regulator ULTRAPETALA1 suppresses de novo root regeneration from Arabidopsis leaf explants

Abstract

Plants have the potency to regenerate adventitious roots from aerial organs after detachment. In Arabidopsis thaliana, de novo root regeneration (DNRR) from leaf explants is triggered by wounding signaling that rapidly induces the expression of the ETHYLENE RESPONSE FACTOR (ERF) transcription factors ERF109 and ABR1 (ERF111). In turn, the ERFs promote the expression of ASA1, an essential enzyme of auxin biosynthesis, which contributes to rooting by providing high levels of auxin near the wounding side of the leaf. Here, we show that the loss of the epigenetic regulator ULTRAPETALA1 (ULT1), which interacts with Polycomb and Trithorax Group proteins, accelerates and reinforces adventitious root formation. Expression of ERF109 and ASA1 was increased in ult1 mutants, whereas ABR1 was not significantly changed. Cultivation of explants on media with exogenous auxin equates adventitious root formation in wild-type with ult1 mutants, suggesting that ULT1 negatively regulates DNRR by suppressing auxin biosynthesis. Based on these findings, we propose that ULT1 is involved in a novel mechanism that prevents overproliferation of adventitious roots during DNRR.

Keywords: ASA1; DNRR; ERF109; adventitious roots; auxin synthesis.

Figure 1.

Loss of ULT1 promotes DNRR. (a-b) Leaf explants of wild-type (Col-0) and ult1-3 mutants, 14 d cultured on B5 media. (c) Rooting rates of Col and ult1-3 leaf explants in a time course. (d) Rooting capacity after 15 d cultured on B5 media. (e) Relative gene expression levels in Col and ult1-3 leaves, 30 min after detachment. (f) Rooting rates of Col and ult1-3 leaf explants after 10 d cultured on B5 media with and without IAA. (g) Rooting capacity after 11 d cultured on B5 media. (h) Conceptional model; JA, jasmonate. (c–g) Asterisks indicate significance, p-value ≤.05; ns indicates no significance (Student t-test).