1. PLETHORA transcription factors orchestrate de novo organ patterning during Arabidopsis lateral root outgrowth
- Author
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Ben Scheres and Yujuan Du
- Subjects
0301 basic medicine ,plant architecture ,Branching ,Cell specification ,Mutant ,Meristem ,education ,Arabidopsis ,Plant Developmental Biology ,DNA-binding protein ,meristem ,Plant Roots ,03 medical and health sciences ,Auxin ,Axis formation ,Gene Expression Regulation, Plant ,branching ,Primordium ,Transcription factor ,chemistry.chemical_classification ,Genetics ,Multidisciplinary ,biology ,Arabidopsis Proteins ,Plant architecture ,fungi ,Lateral root ,food and beverages ,Gene Expression Regulation, Developmental ,cell specification ,Biological Sciences ,biology.organism_classification ,Cell biology ,DNA-Binding Proteins ,030104 developmental biology ,chemistry ,axis formation ,EPS ,Developmental Biology ,Transcription Factors - Abstract
Significance Root architecture is an important trait that is shaped by the formation of primary roots, lateral roots, and adventitious roots. Here, we show that three PLETHORA (PLT) transcription factors are the key molecular triggers for the de novo organ patterning during Arabidopsis lateral root formation. PLT3, PLT5, and PLT7 redundantly regulate the correct initiation of formative cell divisions in incipient lateral root primordia and the proper establishment of gene expression programs that lead to the formation of a new growth axis., Plant development is characterized by repeated initiation of meristems, regions of dividing cells that give rise to new organs. During lateral root (LR) formation, new LR meristems are specified to support the outgrowth of LRs along a new axis. The determination of the sequential events required to form this new growth axis has been hampered by redundant activities of key transcription factors. Here, we characterize the effects of three PLETHORA (PLT) transcription factors, PLT3, PLT5, and PLT7, during LR outgrowth. In plt3plt5plt7 triple mutants, the morphology of lateral root primordia (LRP), the auxin response gradient, and the expression of meristem/tissue identity markers are impaired from the “symmetry-breaking” periclinal cell divisions during the transition between stage I and stage II, wherein cells first acquire different identities in the proximodistal and radial axes. Particularly, PLT1, PLT2, and PLT4 genes that are typically expressed later than PLT3, PLT5, and PLT7 during LR outgrowth are not induced in the mutant primordia, rendering “PLT-null” LRP. Reintroduction of any PLT clade member in the mutant primordia completely restores layer identities at stage II and rescues mutant defects in meristem and tissue establishment. Therefore, all PLT genes can activate the formative cell divisions that lead to de novo meristem establishment and tissue patterning associated with a new growth axis.
- Published
- 2017