A frameshift mutation prevents Kunitz trypsin inhibitor mRNA accumulation in soybean embryos.

Jofuku, K. Diane; Schipper, Rafael; Goldberg, Robert B.

doi:10.1105/tpc.1.4.427

Cited by 111 publications

(61 citation statements)

References 26 publications

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“…In plants, premature termination has been reported to reduce mRNA abundance, presumably by accelerating its decay (Jofuku et al, 1989;Vancanneyt et al, 1990;Voelker et al, 1990;Sullivan and Green, 1993). Discrimination between these alternatives in the Fed-1 system is complicated by the variability in absolute expression between different transgenic lines that is attributable to genomic position effects (Peach and Velten, 1991).…”

Section: Dlscusslonmentioning

confidence: 99%

Light modulation of ferredoxin mRNA abundance requires an open reading frame.

et al. 1994

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Ferredoxin I (Fed-l) mRNA abundance is modulated by an Interna1 light regulatory element that includes sequences both L'and 3'of the translational initiation site. To test the hypothesis that the light response mediated by this element might be coupled to translation, we transformed tobacco plants with gene constructs blocked in translational initiation or elongation. Here, we report that such mutations abollsh the light response ln vivo. A nonsense mutation could be rescued by restorlng the open reading frame with a different sequence, even when the new codon caused an amino acld substitution. Our data establlsh that the light response requires a translatable reading frame and thus pmvide strong circumstantial evidence for post-transcriptional modulation of Fed-1 mRNA levels. The Fed-1 system 1s presently the only higher plant example of a developmentally regulated change in mRNA abundance that requires translation of the affected mRNA. INTRODUCTIONFerredoxin I (Fed-7) is a nuclear gene encoding chloroplast ferredoxin in Pisum (Dobres et al., 1987; Dickey et al., 1992a). Like most genes encoding plastid proteins, Fed-7 is expressed more strongly in the light than in the dark. However, its light response differs in severa1 respects from those of other wellcharacterized light-responsive genes (Kaufman et al., 1986) and involves different molecular events (Thompson, 1988;Thompson and White, 1991;Neuhaus et al., 1993). Among the important differences is the fact that a major light response element in the pea Fed-7 gene is located within the transcription unit (Elliott et al., 1989), while other light-responsive genes are regulated mainly by upstream elements (Thompson and White, 1991;Kuhlemeier, 1992). We have recently shown that the Fed-7 interna1 light regulatory element (iLRE) is located within the 5' portion of the transcribed sequence and that it includes portions of both the leader and coding region (Dickey et ai., 1992b).The location of the Fed-7 iLRE within the transcribed portion of an intronless gene rules out transcriptional regulatory mechanisms that depend on upstream control elements and is consistent with models in which light modulates mRNA abundance by directly or indirectly affecting its rate of degradation. Direct observation of a light effect on mRNA stability has thus far been prevented by the fact that Ad-7 mRNA is stabilized when cellular RNA synthesis is inhibited by actinomycin-D (G.C. Allen, unpublished data). However, other data provide indirect support for a post-transcriptional model. In both tobacco andTo whom correspondence should be addressed.Arabidopsis, changes in mRNA abundance in light-grown versus dark-adapted plants occur in the absence of corresponding changes in the transcriptional activity of isolated nuclei (Dickey et ai., 1992b;Vorst et al., 1993), and the 5' portion of a pea Fed-7::GUS (P-glucuronidase) chimeric mRNA is stabilized in the light, whereas reporter sequences in the 3' portion of the transcript are degraded (Dickey et al., 1992b).Recent reports indicate that ...

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Section: Dlscusslonmentioning

confidence: 99%

Light modulation of ferredoxin mRNA abundance requires an open reading frame.

et al. 1994

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“…This mutation prevents KTi3 mRNA from being translated correctly in embryo cells (Jofuku et al, 1989). Other Kunitz trypsin inhibitor mRNAs (e.g., KTil and KTi2) are unaffected by the frameshift mutation (Jofuku et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

“…We showed previously that the Kunitz trypsin inhibitor gene family is highly regulated during the soybean life cycle (Goldberg et al, 1981;Walling, Drews, and Goldberg, 1986;Jofuku, Schipper, and Goldberg, 1989). These genes are expressed at precise times during embryogenesis, have different expression levels in the embryo cotyledon and axis, and are either inactive or expressed at low levels in mature plant organ systems (Goldberg et al, 1981;Walling et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

“…Jofuku et al (1989) showed that a null line that lacks Kunitz trypsin inhibitor activity has a frameshift mutation in the major Kunitz trypsin inhibitor gene (KTi3). This mutation prevents KTi3 mRNA from being translated correctly in embryo cells (Jofuku et al, 1989). Other Kunitz trypsin inhibitor mRNAs (e.g., KTil and KTi2) are unaffected by the frameshift mutation (Jofuku et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

“…Both transcriptional and posttranscriptional processes regulate Kunitz trypsin inhibitor gene expression (Walling et al, 1986). Jofuku et al (1989) showed that a null line that lacks Kunitz trypsin inhibitor activity has a frameshift mutation in the major Kunitz trypsin inhibitor gene (KTi3). This mutation prevents KTi3 mRNA from being translated correctly in embryo cells (Jofuku et al, 1989).…”

Section: Introductionmentioning

confidence: 99%

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