Abstract Transgenes inserted into the plant genome can become inactive (gene silencing) or result in silencing of homologous cellular genes [homology-dependent gene silencing (HDG silencing)]. In an earlier study we reported HDG silencing of chalcone synthase (CHS) in Arabidopsis. This study concerns genetic revertants of one of the CHS HDG -silencing transgenic homozygotes. Two monogenic recessive trans-acting mutations (hog1 and ddm1) that impair gene silencing and HDG silencing were identified. These mutations reduce genomic DNA methylation and affect the quantity and size of CHS mRNA. These results imply that DNA methylation is necessary for both gene silencing and HDG silencing. Two further monogenic, trans-acting, recessive mutations (sil1 and sil2) reduce gene silencing but not HDG silencing. The existence of this mutant class shows that gene silencing involves genes that are not necessary for HDG silencing. A further mutant (Catt) was isolated and has an attenuated HDG-silencing T-DNA.
Abstract The Arabidopsis hypocotyl, together with hormone mutants and chemical inhibitors, was used to study the role of auxin in cell elongation and its possible interactions with ethylene and gibberellin. When wild-type Arabidopsis seedlings were grown on media containing a range of auxin concentrations, hypocotyl growth was inhibited. However, when axr1-12 and 35S-iaaL(which have reduced auxin response and levels, respectively) were grown in the same conditions, auxin was able to promote hypocotyl growth. In contrast, auxin does not promote hypocotyl growth ofaxr3-1, which has phenotypes that suggest an enhanced auxin response. These results are consistent with the hypothesis that auxin levels in the wild-type hypocotyl are optimal for elongation and that additional auxin is inhibitory. When ethylene responses were reduced using either the ethylene-resistant mutantetr1 or aminoethoxyvinylglycine, an inhibitor of ethylene synthesis, auxin responses were unchanged, indicating that auxin does not inhibit hypocotyl elongation through ethylene. To test for interactions between auxin and gibberellin, auxin mutants were grown on media containing gibberellin and gibberellin mutants were grown on media containing auxin. The responses were found to be the same as wild-type Arabidopsis seedlings in all cases. In addition, 1 μm of the auxin transport inhibitor 1-naphthylphthalmic acid does not alter the response of wild-type seedlings to gibberellin. Double mutants were made between gibberellin and auxin mutants and the phenotypes of these appear additive. These results indicate that auxin and gibberellin are acting independently in hypocotyl elongation. Thus auxin, ethylene, and gibberellin each regulate hypocotyl elongation independently.
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