Poster: Vegetative development

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Abs # 686: Interactions of KNOX, HD-ZIPIII, and miRNA in patterning of vascular meristems in Nicotiana leaves.

Presenter:	Koning, Ross E., Contact Author
Authors	McHale, Neil A. (A)   Koning, Ross E. (B)
Affiliations:	(A): Biochemistry and Genetics Department, Connecticut Agricultural Experiment Station (B): Biology Department, Eastern Connecticut State University
Web Site:	http://plantphys.info

The vascular cambium is an indeterminate tissue positioned between the xylem and phloem, producing vascular initials within leaf midveins and proliferating outward from the lateral flanks to connect the midveins with stem vasculature. In wild-type, cambial development has a distinct orientation and polarity, generating a crescent-shaped midvein (adaxial xylem and abaxial phloem) that curves toward the shoot. Studies in Arabidopsis and Nicotiana show that the pattern of cambial growth depends on miRNA regulation of the HD-ZIPIII pathway. Ectopic abaxial expression of PHAVOLUTA in the absence of miR165/166 regulation (phv1 tobacco mutant) diverts cambial growth away from the shoot, producing adaxialized midveins (xylem surrounding phloem). Exactly the opposite phenotype results from ectopic expression of KNOX genes in the absence of PHANTASTICA function, where cambial growth is misdirected toward the shoot, producing abaxialized midveins (phloem surrounding xylem). One explanation for this abaxializing effect of KNOX is negative regulation of the HD-ZIPIII pathway. We show evidence for this in antisense NsPHAN/phv1 double mutants, where ectopic KNOX suppresses the leaf and midvein phenotypes of the phv1 mutant. KNOX repression of NsPHAV could be mediated through enhanced activity of the miRNA pathway, or through direct transcriptional effects. To look for KNOX influence on domains of miRNA activity, we constructed a 35S::GUS reporter gene carrying a miR165/166 recognition site. Staining patterns are being compared in wild-type and antisense NsPHAN transgenics. A GUS transgene driven by the NsPHAV promoter is also being assayed in wild-type and antisense NsPHAN backgrounds to look for transcriptional repression of the HD-ZIPIII pathway by ectopic KNOX.