|Ph.D Student||Shalit-Kaneh Akiva|
|Subject||From Florigen to Morphogen: Systemic Signals Modulate|
Vegetative/Reproductive Cycles in Plants
|Department||Department of Biology||Supervisors||Professor Emeritus Eliezer Lifschytz|
|Dr. Yuval Eshed|
|Full Thesis text - in Hebrew|
AClassic grafting experiments established a florigenic agent as a major systemic mediator of flowering in photoperiod sensitive plants. Genetic studies in Arabidopsis identified five partially overlapping but organ-autonomous flowering pathways that converge on several integrator genes, notably FT. Studies in tomato provided unequivocal evidence that SFT, the tomato FT orthologue, generates graft-transmissible signals that induce flowering in long, short and day-neutral plants and are epistatic to all known late flowering mutant genes. In this work we established that in addition to its role in flowering florigen functions as a long-range regulator of meristematic potentials in every above ground organ by shifting the balance from growth to termination. To this effect florigen targets an endogenous organ and tissue specific ratio between SINGLE FLOWER TRUSS (SFT) and its potent antagonist SELF PRUNNING (SP). SFT promotes meristem termination and flowering whereas SP promotes growth and delays flowering. Both genes are of the CETS family coding for small globular proteins with a potential anionic binding pocket. In the SAMs the plant uses this upper regulatory tier to promote flowering differentially in primary and secondary shoots thus patterning the reiterative growth/termination cycles of tomato typical to perennial plants. In addition however we show that florigen modulates the SFT/SP ratio in all known vegetative meristems therefore determining the size of the stem, compound leaf complexity, the formation of floral abscission zone and the balance between apical dominance and sympodial branching.
Because a major effect of florigen is to attenuate meristems and its upregulation results in deleterious growth effects that are moderated by SP in an SFT-dependent manner, we suggested that the evolution of SP as a functional antagonist of florigen evolved concomitantly with the potential of florigen to induce abrupt arrest of vegetative apical meristems. Indeed, cladistic analysis of all available CETS genes from basal and flowering land plants suggested that the SP/TFL1 clade of the CETS family is a new innovation of flowering plants. Moreover, transgenic plants over expressing FT-Like genes from gymnosperms do not mimic florigen but rather SP, strengthening our hypothesis as to the SFT/SP system's novelty in flowering plants. Our current model holds that the FT protein and its orthologs in all flowering plants are the universal genetic origin of the florigenic signal and that this function is a subset of the roles florigen is playing as a general growth hormone and a long range regulator of all above ground meristems.