The controlling element Ds at the Shrunken locus in Zea mays: Structure of the unstable sh-m5933 allele and several revertants

A tissue-specific epistatic mode of gene interaction was observed between molecularly homologous genes Sh1 and Sus1 (hereafter, Sh and Sus), encoding the sucrose synthase (SS) isozymes, SS1 and SS2, respectively. In Sh Sus genotype, both SS genes were expressed simultaneously and approximately equally in young seedlings; however, only the Sus-encoded SS2 protein was seen in the developing embryos. By contrast, the mutant sus genotype, lacking detectable levels of the SS2 protein in various tissues tested, showed expression of the Sh locus as judged by the detection of the SS1 protein in such embryos. Ectopic expression in embryos was seen from two separate Sh alleles, Sh-W22 and Sh'-5 (a revertant allele derived upon Ds excision from sh-m5933). In each case, the Sh expression at the protein level in embryos was unique to genotypes with the mutant sus gene. Based on the observed lack of phenotypic change in the sus mutant, we suggest that the ectopic expression of the Sh in otherwise Sus-specific tissues leads to functional compensation. There was no epistatic interaction of Sh and Sus at the RNA level as SS1 transcripts were detectable in both Sus and sus embryos. Thus, embryo specificity between the two SS genes was determined at posttranscriptional or at translational level of control. We surmise on the basis of these data that metabolic regulatory controls seem to override the normal constraints of tissue and cell specificity of the nonallelic isozyme genes to maintain efficient use of the pathways.

Section: Isolation and Characterization Of The Specific Genotypesmentioning

confidence: 99%

Epistatic interaction and functional compensation between the two tissue- and cell-specific sucrose synthase genes in maize.

Chourey¹,

Taliercio²

1994

“…Transposon insertions can alter transcription and transcript processing, and there are cases in which transposons are processed out of transcripts by virtue of the presence of splice donor and acceptor sequences (43)(44)(45). Transposons also can promote the movement of large segments of DNA either by transposition or by illegitimate recombination (46,47).…”

Section: What Do Transposons Do?mentioning

confidence: 99%

Transposons and genome evolution in plants

Fedoroff

2000

158

Although it is known today that transposons comprise a significant fraction of the genomes of many organisms, they eluded discovery through the first half century of genetic analysis and even once discovered, their ubiquity and abundance were not recognized for some time. This genetic invisibility of transposons focuses attention on the mechanisms that control not only transposition, but illegitimate recombination. The thesis is developed that the mechanisms that control transposition are a reflection of the more general capacity of eukaryotic organisms to detect, mark, and retain duplicated DNA through repressive chromatin structures.

“…These mechanisms have in common that terminal inverted repeats (TIR) of different transposons, located on either the same or different sister chromatids, serve as substrates for transposase. For Ac͞Ds, most reports associate chromosomal rearrangements such as deletions with elements of complex structure (11)(12)(13)(14)(15)(16)(17), whereas single simple Ds elements are commonly not believed to cause chromosomal rearrangements (18). Unequal homologous recombination where transposable elements serve as dispersed sites of sequence homology is the major recombination mechanism known to cause transposon-induced deletions (19,20).…”

mentioning

confidence: 99%

Intrachromosomal excision of a hybrid Ds element induces large genomic deletions in Arabidopsis

Page

Köhler

Costa-Nunes

et al. 2004

Transposon activity is known to cause chromosome rearrangements in the host genome. Surprisingly, extremely little is known about Dissociation (Ds)-induced chromosome rearrangements in Arabidopsis, where Ds is intensively used for insertional mutagenesis. Here, we describe three Arabidopsis mutants with reduced fertility and propose that excision of a hybrid Ds element induced a large genomic deletion flanking Ds. In the mutants anat and haumea, the deletion mechanism consists of a local Ds transposition from replicated into unreplicated DNA followed by Ds excision, where one end of the newly transposed element and one end of the Ds transposon at the donor site served as substrate for transposase. Excision of this hybrid element reminiscent of a macrotransposon leads to loss of the chromosomal piece located between the two ends, including one full Ds element and the flanking genomic sequence. This mechanism was found to be responsible for several other deletions and occurs at a genetically trackable frequency. Thus, it could be applied to efficiently generate deletions of various sizes in the vicinity of any existing Ds element present in the genome. In the mutant tons missing, a mechanism that involves endogenous repetitive sequences caused a large flanking deletion at a position unlinked to the starter locus. Our study of Ds transposition in Arabidopsis revealed previously undescribed mechanisms that lead to large genomic deletions flanking Ds elements, which may contribute to genome dynamics and evolution. genome evolution ͉ rearrangements ͉ transposition