Exocyst mutants suppress pollen tube growth and cell wall structural defects of hydroxyproline O‐arabinosyltransferase mutants

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/1/tpj14808-sup-0003-FigS3.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/9/tpj14808.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/8/tpj14808-sup-0001-FigS1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/7/tpj14808-sup-0004-FigS4.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/6/tpj14808-sup-0005-FigS5.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/5/tpj14808-sup-0007-FigS7.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/4/tpj14808-sup-0006-FigS6.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/3/tpj14808-sup-0002-FigS2.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/156472/2/tpj14808_am.pd

Synchronization of the flowering transition by the tomato TERMINATING FLOWER gene

The transition to flowering is a major determinant of plant architecture, and variation in the timing of flowering can have profound effects on inflorescence architecture, flower production and yield. Here, we show that the tomato mutant terminating flower (tmf) flowers early and converts the multiflowered inflorescence into a solitary flower as a result of precocious activation of a conserved floral specification complex encoded by ANANTHA (AN) and FALSIFLORA (FA). Without TMF, the coordinated flowering process is disrupted, causing floral identity genes, such as AN and members of the SEPALLATA (SEP) family, to activate precociously, while the expression of flowering transition genes, such as FRUITFULL (FUL), is delayed. Indeed, driving AN expression precociously is sufficient to cause early flowering, and this expression transforms multiflowered inflorescences into normal solitary flowers resembling those of the Solanaceae species petunia and tobacco. Thus, by timing AN activation, TMF synchronizes flower formation with the gradual reproductive transition, which, in turn, has a key role in determining simple versus complex inflorescences

A cascade of arabinosyltransferases controls shoot meristem size in tomato

Shoot meristems of plants are composed of stem cells that are continuously replenished through a classical feedback circuit involving the homeobox WUSCHEL (WUS) gene and the CLAVATA (CLV) gene signaling pathway. In CLV signaling, the CLV1 receptor complex is bound by CLV3, a secreted peptide modified with sugars. However, the pathway responsible for modifying CLV3 and its relevance for CLV signaling are unknown. Here we show that tomato inflorescence branching mutants with extra flower and fruit organs due to enlarged meristems are defective in arabinosyltransferase genes. The most extreme mutant is disrupted in a hydroxyproline O-arabinosyltransferase and can be rescued with arabinosylated CLV3. Weaker mutants are defective in arabinosyltransferases that extend arabinose chains, indicating that CLV3 must be fully arabinosylated to maintain meristem size. Finally, we show that a mutation in CLV3 increased fruit size during domestication. Our findings uncover a new layer of complexity in the control of plant stem cell proliferation