Liriodendron chinense LcMAX1 regulates primary root growth and shoot branching in Arabidopsis thaliana

Strigolactones (SLs) play prominent roles in regulating shoot branching and root architecture in model plants. However, their roles in non-model (particularly woody) plants remain unclear. Liriodendron chinense is a timber tree species widely planted in southern China. The outturn percentage and wood quality of L. chinense are greatly affected by the branching characteristics of its shoot, and the rooting ability of the cuttings is key for its vegetative propagation. Here, we isolated and analyzed the function of the MORE AXILLARY GROWTH 1 (LcMAX1) gene, which is involved in L. chinense SL biosynthesis. RT-qPCR showed that LcMAX1 was highly expressed in the roots and axillary buds. LcMAX1 was located in the endoplasmic reticulum (ER) and nucleus. LcMAX1 ectopic expression promoted primary root growth, whereas there were no phenotypic differences in shoot branching between transgenic and wild-type (WT) A. thaliana plants. LcMAX1 overexpression in the max1 mutant restored them to the WT A. thaliana phenotypes. Additionally, AtPIN1, AtPIN2, and AtBRC1 expressions were significantly upregulated in transgenic A. thaliana and the max1 mutant. It was therefore speculated that LcMAX1 promotes primary root growth by regulating expression of auxin transport-related genes in A. thaliana, and LcMAX1 inhibits shoot branching by upregulating expression of AtBRC1 in the max1 mutant. Altogether, these results demonstrated that the root development and shoot branching functions of LcMAX1 were similar to those of AtMAX1. Our findings provide a foundation for obtaining further insights into root and branch development in L. chinense.

Automated summary

The LcMAX1 gene in Liriodendron chinense is involved in root and shoot development, similar to the function of AtMAX1 in Arabidopsis thaliana. LcMAX1 promotes primary root growth by regulating auxin transport-related genes, while inhibiting shoot branching by upregulating the expression of AtBRC1 in the max1 mutant.