Organization of paramutagenicity in R-stippled maize.

Abstract

In heterozygotes, R-stippled (R-st) reduces the pigmenting potential of sensitive r alleles heritably (paramutation). R-st is comprised of four r genes arranged in direct orientation. Unequal crossing over within R-st generates deletion products retaining from one to three r genes. Paramutagenic strength decreased in parallel with copy number, both among internal and distal deletions. Single-gene R-st derivatives were nonparamutagenic. This was so whether or not the single gene retained the transposable element (I-R) responsible for seed spotting. Adding back r genes by intragenic recombination increased paramutagenicity in proportion to total gene number. Each member of a set of overlapping deletions retained moderately strong activity, showing that no single r gene or intragenic region is required for paramutagenicity. Proximal and distal loss R-st derivatives, each retaining two r genes, were less paramutagenic in trans than the corresponding four copy cis combination, indicating R-st's paramutagenic determinants function as a cis-interdependent unit in bringing about modification of a sensitive allele.

Transgene-Induced Silencing Identifies Sequences Involved in the Establishment of Paramutation of the Maize p1 Gene

“…In some cases, different chromosomal components may be involved in paramutagenicity versus paramutability. At the maize r1 locus, for example, the relative paramutagenic strength of recombinant alleles derived from R1-mb and R1-st is proportional to the number of R1 gene repeats that each contains (Kermicle et al, 1995;Panavas et al, 1999), whereas paramutability of the R1-r allele requires a small (300 bp) sequence named that is located between two divergently transcribed r1 gene copies (Walker et al, 1995;Kermicle, 1996). The region contains remnants of the transposon doppia, the subterminal repeats of which were proposed to serve as targets of paramutagenic modification(s) (Walker, 1998).…”

“…For r1 paramutation, the relationship between the degree of suppression and paramutagenicity is more difficult to assess. Paramutagenic R1-st and R1-mb are complex alleles; each contains functional r1 gene copies that may obscure phenotypic suppression of the paramutagenic copies (Eggleston et al, 1995;Kermicle et al, 1995;Panavas et al, 1999). One of the distinguishing characteristics of different paramutation systems is the stability of the paramutable and paramutagenic alleles.…”

“…Repeated sequences have been implicated in several epigenetic phenomena, including paramutation (Assaad et al, 1993;Kermicle et al, 1995;Meyer, 1996;Ye and Signer, 1996;Dorer and Henikoff, 1997;Panavas et al, 1999). In r1 paramutation, both paramutagenic alleles, R1-st (Eggleston et al, 1995;Kermicle et al, 1995) and R1-mb (Panavas et al, 1999), have repetitive structures that are crucial for their paramutagenicity.…”

“…Repeated sequences have been implicated in several epigenetic phenomena, including paramutation (Assaad et al, 1993;Kermicle et al, 1995;Meyer, 1996;Ye and Signer, 1996;Dorer and Henikoff, 1997;Panavas et al, 1999). In r1 paramutation, both paramutagenic alleles, R1-st (Eggleston et al, 1995;Kermicle et al, 1995) and R1-mb (Panavas et al, 1999), have repetitive structures that are crucial for their paramutagenicity. A decreased number of tandem copies of r1 genes in recombinant R1-st or R1-mb alleles leads to diminished paramutagenicity, with single-copy alleles being nonparamutagenic (Kermicle et al, 1995;Panavas et al, 1999).…”

“…In r1 paramutation, both paramutagenic alleles, R1-st (Eggleston et al, 1995;Kermicle et al, 1995) and R1-mb (Panavas et al, 1999), have repetitive structures that are crucial for their paramutagenicity. A decreased number of tandem copies of r1 genes in recombinant R1-st or R1-mb alleles leads to diminished paramutagenicity, with single-copy alleles being nonparamutagenic (Kermicle et al, 1995;Panavas et al, 1999). Similar observations indicate the importance of repetitive structures for the paramutagenicity of a transgene locus (H2) in tobacco (Jakowitsch et al, 1999).…”