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. 2006 Jul 10;103(29):11081–11085. doi: 10.1073/pnas.0602038103

Fig. 3.

Fig. 3.

Phenotypes of crf loss-of-function mutations. (A) Representative whole seedlings and a close-up of cotyledons. CRF mutant cotyledon defects increase in severity from a notch in the single mutants to an extreme lack of cell expansion of the triple mutant. The cytokinin triple receptor knockout mutant ahk2,ahk3,ahk4 also has small cotyledons, but no shape abnormality. (Scale bar, 1 mm.) (B) The double crf5,crf6 mutant is embryo lethal. Wild-type and single crf5 and crf6 mutant allele siliques display complete seed set, whereas the self-set (⊗) siliques of crf5/crf5,CRF6/crf6 or CRF5/crf5,crf6/crf6 individuals result in ≈25% aborted seeds. The transgenic addition of CRF5 cDNA complements the embryo lethal phenotype in a crf5/crf5,crf6/crf6 double mutant background. (C) Developing embryos, shown from a self-fertilized (⊗) crf5/crf5,CRF6/crf6 plant, reveals ≈25% of the embryos fail to develop past the early heart stage.