Escape From Repeat-Induced Point Mutation of a Gene-Sized Duplication in Neurospora crassa Crosses That Are Heterozygous for a Larger Chromosome Segment Duplication

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1581-1590 ◽  
Author(s):  
Ashwin Bhat ◽  
Durgadas P Kasbekar
Keyword(s):  
Transposable Element ◽  
Neurospora Crassa ◽  
Point Mutation ◽  
Target Gene ◽  
The Other ◽  
Chromosome Segment ◽  
Chromosome Segment Duplications ◽  
Repeat Induced Point Mutation

Abstract In Neurospora crassa the ability of an ectopic gene-sized duplication to induce repeat-induced point mutation (RIP) in its target gene was suppressed in crosses that were heterozygous for another larger chromosome segment duplication. Specifically, the frequency of RIP in the erg-3 gene due to a 1.3-kb duplication was reduced if the chromosome segment duplications Dp(IIIR > [I;II]) AR17, Dp(VIR > IIIR) OY329, or Dp(IVR > VII) S1229 were present in either the same or the other parental nucleus of the premeiotic dikaryon. We suggest that the larger duplications act as sinks to titrate the RIP machinery away from the smaller duplication. In contrast, RIP efficiency was relatively unaffected in comparably unproductive interspecies crosses with N. intermedia and N. tetrasperma. These findings offer a novel explanation for the observed persistence of the transposable element Tad in only a subset of Neurospora strains.

scholarly journals The Neurospora transposon Tad is sensitive to repeat-induced point mutation (RIP).

Genetics ◽  
1994 ◽  
Vol 138 (3) ◽  
pp. 657-664
Author(s):  
J A Kinsey ◽  
P W Garrett-Engele ◽  
E B Cambareri ◽  
E U Selker
Keyword(s):  
Life Cycle ◽  
Transposable Element ◽  
Neurospora Crassa ◽  
Point Mutation ◽  
Repeated Sequences ◽  
Active Line ◽  
Common Laboratory ◽  
Repeat Induced Point Mutation

Abstract RIP (repeat-induced point mutation) efficiently mutates repeated sequences in the sexual phase of the Neurospora crassa life cycle. Nevertheless, an active LINE-like retrotransposon, Tad, was found in a N. crassa strain from Adiopodoumé. The possibility was tested that Tad might be resistant to RIP, or that the Adiopodoumé strain might be incompetent for RIP. Tad elements derived from the Adiopodoumé strain were found to be susceptible to RIP. In addition, strains lacking active Tad elements, including common laboratory strains and strains representing seven species of Neurospora, were found to have sequences closely related to Tad but with numerous mutations of the type resulting from RIP (G:C to A:T). Even the Adiopodoumé strain showed Tad-like elements with mutations characteristic of RIP. Results of crossing of an Adiopodoumé transformant with progeny of Adiopodoumé suggest that the Adiopodoumé strain is proficient at RIP. We conclude that Tad is an old transposable element that has been inactivated by RIP in most strains. Finding relics of RIP in both heterothallic and homothallic species of Neurospora implicates RIP across the genus.

scholarly journals Synthesis of Signals for De Novo DNA Methylation in Neurospora crassa

2003 ◽  
Vol 23 (7) ◽  
pp. 2379-2394 ◽  
Author(s):  
Hisashi Tamaru ◽  
Eric U. Selker
Keyword(s):  
Dna Methylation ◽  
Neurospora Crassa ◽  
Point Mutation ◽  
Dna Sequences ◽  
De Novo ◽  
Test Site ◽  
Minor Groove ◽  
Binding Motif ◽  
Repeat Induced Point Mutation

ABSTRACT Most 5-methylcytosine in Neurospora crassa occurs in A:T-rich sequences high in TpA dinucleotides, hallmarks of repeat-induced point mutation. To investigate how such sequences induce methylation, we developed a sensitive in vivo system. Tests of various 25- to 100-bp synthetic DNA sequences revealed that both T and A residues were required on a given strand to induce appreciable methylation. Segments composed of (TAAA) n or (TTAA) n were the most potent signals; 25-mers induced robust methylation at the special test site, and a 75-mer induced methylation elsewhere. G:C base pairs inhibited methylation, and cytosines 5′ of ApT dinucleotides were particularly inhibitory. Weak signals could be strengthened by extending their lengths. A:T tracts as short as two were found to cooperate to induce methylation. Distamycin, which, like the AT-hook DNA binding motif found in proteins such as mammalian HMG-I, binds to the minor groove of A:T-rich sequences, suppressed DNA methylation and gene silencing. We also found a correlation between the strength of methylation signals and their binding to an AT-hook protein (HMG-I) and to activities in a Neurospora extract. We propose that de novo DNA methylation in Neurospora cells is triggered by cooperative recognition of the minor groove of multiple short A:T tracts. Similarities between sequences subjected to repeat-induced point mutation in Neurospora crassa and A:T-rich repeated sequences in heterochromatin in other organisms suggest that related mechanisms control silent chromatin in fungi, plants, and animals.

RIP (repeat induced point mutation) as a tool in the analysis of P-450 and sterol biosynthesis in Neurospora crassa

1991 ◽  
Vol 19 (3) ◽  
pp. 799-802 ◽  
Author(s):  
Ian F. Connerton ◽  
Shelly M. Deane ◽  
Jenny A. Butters ◽  
R. S. Thomas Loeffler ◽  
Derek W. Hollomon
Keyword(s):  
Neurospora Crassa ◽  
Point Mutation ◽  
Sterol Biosynthesis ◽  
Repeat Induced Point Mutation
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