Higuchi et al. 10.1073/pnas.0402887101. |
Fig. 10. (A) RT-PCR analysis of CRE-family genes in mutant backgrounds. RT-PCR was performed on cDNA prepared from 10 ng of total RNA from Columbia WT (lanes 1, 3, 5, and 7), cre1-12 (lanes 2 and 8), ahk2-2 (lanes 4 and 9) and ahk3-3 (lanes 6 and 10). Primers specific to CRE1 (lanes 1 and 2), AHK2 (lanes 3 and 4), AHK3 (lanes 5 and 6) and AtIPT9 (lanes 7-10) were used for amplification of the appropriate transcript. AtIPT9 was used as a control for cDNA amplification. (B) Schematic representation of the T-DNA insertion locations. Boxes represent exons, horizontal bars introns, and triangles T-DNA integration sites. DNA regions corresponding to the primers used for RT-PCR in A are shown as open arrows. Filled regions correspond to exon sequences, unfilled regions intron sequences. (C) Sequencing of the T-DNA/plant genomic DNA junctions in the CRE-family mutant alleles. Boxes represent the T-DNA insert, LB the left border of the T-DNA, RB the right border of the T-DNA.
Fig. 11. Adult phenotypes of all possible mutant combinations within the CRE family. Plants were grown on soil, in the absence of cytokinin. (Bars = 10 mm.)
Fig. 12. Induction of shoot and root formation on hypocotyl-derived callus tissue from cytokinin receptor mutants.
Fig. 13. FACS data for root cells. (A) WT Columbia. (B) cre1-12 ahk2-2 ahk3-3 triple mutant.