PT  - JOURNAL ARTICLE
AU  - Yang Li
AU  - Rihua Lei
AU  - Mengna Pu
AU  - Yuerong Cai
AU  - Chengkai Lu
AU  - Zhifang Li
AU  - Gang Liang
TI  - bHLH11 inhibits bHLH IVc proteins by recruiting the TOPLESS/TOPLESS-RELATED corepressors in Arabidopsis
AID  - 10.1101/2020.04.09.035097
DP  - 2022 Jan 01
TA  - bioRxiv
PG  - 2020.04.09.035097
4099  - http://biorxiv.org/content/early/2022/02/11/2020.04.09.035097.short
4100  - http://biorxiv.org/content/early/2022/02/11/2020.04.09.035097.full
AB  - Iron (Fe) homeostasis is essential for plant growth and development. Many transcription factors play pivotal roles in the maintenance of Fe homeostasis. bHLH11 was identified as a negative transcription factor regulating Fe homeostasis, however, the underlying molecular mechanism remains elusive. We generated two loss-of-function bhlh11 mutants which display the enhanced sensitivity to Fe excess, the increased Fe accumulation and the elevated expression of Fe deficiency responsive genes. bHLH11 protein, localized in both the cytoplasm and nucleus, decreases in response to Fe deficiency. Coexpression assays indicate that bHLH IVc transcription factors (TFs) (bHLH34, bHLH104, bHLH105, and bHLH115) facilitate the nuclear accumulation of bHLH11 protein. Further analysis indicates that bHLH11 represses the transactivity of bHLH IVc TFs towards bHLH Ib genes (bHLH38, bHLH39, bHLH100, and bHLH101). bHLH11 contains two EAR motifs which are responsible for the repression function by recruiting the TOPLESS/TOPLESS-RELATED (TPL/TPRs) corepressors. Correspondingly, the expression of Fe uptake genes increases in the tpr1 tpr4 tpl mutant. Moreover, genetic analysis reveals that bHLH11 has functions independent of FIT. This study provides insights into the complicate Fe homeostasis signaling network.One-sentence summary bHLH IVc proteins promote the bHLH11 protein accumulation in the nucleus where bHLH11 inhibits the transcriptional activation ability of bHLH IVc via its EAR motifs recruiting the TOPLESS/TOPLESS-RELATED corepressors.Competing Interest StatementThe authors have declared no competing interest.