Final Report Summary - PLT (PLETHORA transcriptions factors, new players in the control of phyllotaxis in Arabidopsis thaliana)
In plants, the shoot apical meristem (SAM), located at the tip of the stem, is the source of all above ground post embryonic organs. The SAM arises during embryogenesis and operates throughout the life of the plant to maintain a self-renewed population of undifferentiated stem cells and to generate different types of organs. Lateral organs, such as leaves and flowers, follow a regular pattern, or phyllotaxis, that can be described mathematically and defines part of the plant architecture.
One of the most abundant lateral organ pattern in nature is the spiral phyllotaxis, found in the plant model Arabidopsis thaliana. This pattern is described by successive organs along the stem being separated by the so called 'golden angle' 137.5°. Recently we reported that in Arabidopsis, the triple loss-of-function mutant plethora3, plethora5, plethora7 (plt3plt5plt7) is defective in establishing spiral phyllotaxis and preferentially adopts a distichous pattern of lateral organ initiation where organs form sequentially separated by 180°. PLT3, PLT5 and PLT7 genes encode for AP2 domain transcription factors. Phyllotaxis is known to be dependent on the phytohormone auxin polarised transport; however, what parameters control precise switch in phyllotaxis are unknown.
Using a domain specific complementation approach, I demonstrated that PLT's function in the centre of the meristem is required and sufficient for organ patterning. During this project, I showed that auxin biosynthesis is reduced in the apex of plt3plt5plt7, and mutants with reduced auxin biosynthesis leads to a similar phenotype as plt3plt5plt7. Moreover, expression of the auxin biosynthetic gene YUCCA4 in the centre of plt3plt5plt7 meristem fully complements the triple mutant phyllotactic phenotype. Therefore, PLT transcription factors regulate auxin biosynthesis throughout the meristem, controlling the quantity of auxin available for organ initiation and patterning. The observation of central zone markers showed that the stem cell niche sise is reduced in plt3plt5plt7 mutant background. Increasing the sise of the stem cell niche by increasing the phytohormone cytokinin biosynthesis in plt3plt5plt7 background is also sufficient to rescue the organ patterning defect of the mutant. Expression analysis of marker genes showed that the rescue of plt3plt5plt7 observed with cytokinin biosynthesis is not correlated to a larger stem cell niche, but to a higher auxin production. Together these data show that PLT-mediated control of auxin biosynthesis in the SAM regulates phyllotaxis. Furthermore, this work emphasises the tight cross regulation between cytokinin and auxin biosynthesis to couple stem cell fate to organogenesis and phyllotaxis.
