Qin Heji Research Group of School of Life Sciences discovered important new components of plant cytokinin signaling pathways

Plant hormones play a very important role
in regulating plant plasticity development.
Developments in plant genetics and molecular biology have led to the resolution
of signaling pathways for many important plant hormones, including auxin, cytokinin, gibberellin, ethylene, abscisic acid, jasmonin, rapeolactone, and monolide 。 It has been found that multiple hormone signaling pathways use similar regulatory mechanisms to accurately regulate the output of hormone signals, such as auxin, jasmine and monocle goldenolactone signaling pathways are all regulated by transcriptional inhibitors containing EAR motifs such as AUX/IAA, JAZ-NINJA and D53/SMXL recruitment co-inhibitors TPL/TPRs to finely control the role of hormones (1-4).

。 In the signaling pathway of these hormones, hormones promote the degradation of transcription inhibitors containing EAR motifs such as AUX/IAA, JAZ and D53/SMXL, thereby lifting the inhibition of transcription factors such as ARF, MYC and IPA by the complex formed by these inhibitors and TPL/TPRs, thereby activating the hormone signaling pathway
.
In addition, ERFs in the ethylene signaling pathway, AFPs in the abscisic acid signaling pathway, and BZR1 and BES1 in the rapetin lactone signaling pathway also contain typical EAR transcriptional inhibition motifs
.
However, it is unclear whether the cytokinin signaling pathway is regulated by transcriptional inhibitors containing the EAR motif (5).

On September 9, 2022, Professor Qin Heji's research group at the School of Life Sciences of Peking University published important progress in Science Advances under the title of "Arabidopsis TIE1 and TIE2 transcriptional repressors dampen cytokinin response during root development".

When Professor Qin Heji's research group studied the TIE transcriptional inhibitor family function discovered and named by his research group, he found that when the TIE1 or TIE2 genes were knocked out at the same time in Arabidopsis, the main root of the plant became significantly shorter, and the number of lateral roots was also significantly reduced, which seriously affected the morphological development of the roots (Figure 1A); The T-DNA overexpression of TIE1 inserts the main root that activates the mutant tie1-D becomes longer and the number of lateral roots increases (Figure 1B
).

The study not only discovered the key component of the cytokinin signaling pathway, TIE transcription inhibitor, but also revealed the molecular mechanism by which TIE regulates the plasticity development of cytokinin signaling pathways and roots, that is, when cells sense cytokinin signaling through cytokinin receptors AHKs, autophosphorylation occurs on their histidine, followed by the transfer of phosphate groups to their aspartate residues, activating their function by phosphorylation type B ARRs by AHPs, type B In addition to regulating the expression of numerous genes that respond to cytokinins, ARRs bind to the TIE1 and TIE2 promoter regions to promote their expression, and TIE1 and TIE2 interact with type B ARRs, inhibit their activity, and close the signaling pathway in time when there is no cytokinin signal input (Figure 1C
).

Figure 1.
A.
Morphology
of roots after 14 d of vertical culture of wild-type and tie1-1 tie2-1 mutants.
The phenotype of tie1-1 tie2-1 mutant roots is significantly shorter than that of the wild type, and the lateral roots are also less than those of the
wild type.
B.
Morphology
of roots after 9 d of wild type and tie1-D vertical culture.
T-DNA insertion activating mutants that overexpress TIE1 are significantly longer than those of the wild type, and there are also more
lateral roots.
C.
Working mode diagram
of TIE transcription inhibitor regulating cytokinin signaling pathways.
When plants sense the important hormone cytokinin signal through the cytokinin receptor AHKs, autophosphorylation occurs on its histidine first, followed by the transfer of phosphate groups to its aspartate residue, which activates its function by phosphorylation type B ARRs by AHPs, type B ARRs, in addition to regulating the expression of numerous genes that respond to cytokinins, also binds to the TIE1 and TIE2 promoter regions to promote their expression, and TIE1 and TIE2 interact with type B ARRs , inhibits its activity, shuts down the signal pathway in time when there is no cytokinin signal input, avoids overreaction of plants to cytokinin signal

He Qinghe, a doctoral student at Peking University, and Dr.
Rongrong, a graduate, are co-first authors
of the paper.
Qin Heji is the corresponding author
of the paper.
Graduated from Peking University, Dr.
Zhang Tiantian, Dr.
Lan Jingqiu, and teacher An Fengying also participated in the work
.
The research was supported
by the National Natural Science Foundation of China (31725005), the Innovation Group (31621001), and the State Key Laboratory of Protein and Plant Genetics Research.

Qin Heji's research group has long been committed to studying leaf development and finding important common conservative regulatory mechanisms
that control the development of plant organs.
In recent years, through molecular genetics and biochemistry, it has been found that a number of genes play an important role in regulating the plasticity development of organs such as leaves, including transcription factors (TCP and WRKY, etc.
), TCP and transcription inhibitors, and the TCP/TIE/TEAR regulatory module formed by E3 ubiquitin ligase to fine-regulate the plasticity development of leaves, epidermal hair, branches and ovules (Plant Cell, 2013; Cell Research, 2015; Plant Cell, 2015; Plant Cell, 2017; PloS Genetics, 2018; New Phytologist, 2018; iScience, 2019; Plant Physiology, 2021; Plant Communication, 2022), the type B ARR-TIE-TPL/TPRs regulatory module regulates the mechanism of plant root plasticity development by fine-control of cytokinin signaling pathways in a good parallel with the mechanism of TCP-TIE-TPL/TRs regulating leaf plasticity development, which is an important advance
in the field of cytokinin and organ plasticity development.

References

（1）H.

（2）L.

（3）L.

（4）L.

（5）J.