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Identification of Inverse Regulator-a (Inr-a) as Synonymous with Pre-mRNA Cleavage Complex II Protein (Pcf11) in Drosophila.

Xie W, Birchler JA - G3 (Bethesda) (2012)

Bottom Line: Such effects can be reduced to the action of single genes.One gene previously found to modulate leaky alleles of the white eye color gene in Drosophila is Inverse regulator-a (Inr-a).The identification of the molecular lesion of Inr-a provides insight into the basis of this common aneuploidy effect.

View Article: PubMed Central - PubMed

Affiliation: Division of Biological Sciences, University of Missouri-Columbia, Columbia, Missouri 65211.

ABSTRACT
A common modulation of gene expression in aneuploids is an inverse correlation of the monitored gene with the dosage of another segment of the genome. Such effects can be reduced to the action of single genes. One gene previously found to modulate leaky alleles of the white eye color gene in Drosophila is Inverse regulator-a (Inr-a). Heterozygotes of mutations increase the expression of white about 2-fold, and trisomic regions surrounding the gene reduce the expression to about two-thirds of the normal diploid level. Further cytological definition of the location of this gene on the second chromosome led to a candidate pre-mRNA cleavege complex II protein (Pcf11) as the only gene in the remaining region whose mutations exhibit recessive lethality as do alleles of Inr-a. The product of Pcf11 has been implicated in transcriptional initiation, elongation, and termination reactions. Four mutant alleles showed molecular lesions predicted to lead to nonfunctional products of Pcf11. The identification of the molecular lesion of Inr-a provides insight into the basis of this common aneuploidy effect.

No MeSH data available.


Lesions identified in the Pcf11 gene from the Inr-a mutations. (A) A stop codon found in the Inr-aEMS-2/+ heterozygote. A base pair of C:G was changed to T:A by EMS mutagenesis, thus changing 456R to a stop codon (Z). The double peaks indicate a nucleotide change. DNA sequence and its translation are shown. (B) A replacement of 7 bp with 5 bp (colored in DNA sequences) was found in the Inr-aγC/+ heterozygote. A series of double peaks is shown. The original and new DNA sequences and the translation of the original one are indicated. (C). Double peaks were found in Pcf11 intron 4 in the Inr-ahd1/+ heterozygote. This change is in the conserved splicing donor site (shaded). DNA sequences of the exon intron were shown as upper- and lowercased letters.
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fig2: Lesions identified in the Pcf11 gene from the Inr-a mutations. (A) A stop codon found in the Inr-aEMS-2/+ heterozygote. A base pair of C:G was changed to T:A by EMS mutagenesis, thus changing 456R to a stop codon (Z). The double peaks indicate a nucleotide change. DNA sequence and its translation are shown. (B) A replacement of 7 bp with 5 bp (colored in DNA sequences) was found in the Inr-aγC/+ heterozygote. A series of double peaks is shown. The original and new DNA sequences and the translation of the original one are indicated. (C). Double peaks were found in Pcf11 intron 4 in the Inr-ahd1/+ heterozygote. This change is in the conserved splicing donor site (shaded). DNA sequences of the exon intron were shown as upper- and lowercased letters.

Mentions: Next, we amplified the genomic DNA and sequenced the Pcf11 gene of three Inr-a heterozygous mutants available in our lab stocks described in Materials and Methods. A stop codon mutation was found in the mutation Inr-aEMS-2, which changes 456R (according to Pcf11-PD) to a stop codon (CGA to UGA in exon 6) (Figure 2A; see Figure 1B for its location in the gene). A frame-shift mutation was found in Inr-aγC: seven base pairs (bp)(TTGCTCC) are replaced by five (GCGCA) in exon 7; thus the amino acid sequence is changed after 656 K (see Figure 2B; see Figure 1B for its location in the gene).


Identification of Inverse Regulator-a (Inr-a) as Synonymous with Pre-mRNA Cleavage Complex II Protein (Pcf11) in Drosophila.

Xie W, Birchler JA - G3 (Bethesda) (2012)

Lesions identified in the Pcf11 gene from the Inr-a mutations. (A) A stop codon found in the Inr-aEMS-2/+ heterozygote. A base pair of C:G was changed to T:A by EMS mutagenesis, thus changing 456R to a stop codon (Z). The double peaks indicate a nucleotide change. DNA sequence and its translation are shown. (B) A replacement of 7 bp with 5 bp (colored in DNA sequences) was found in the Inr-aγC/+ heterozygote. A series of double peaks is shown. The original and new DNA sequences and the translation of the original one are indicated. (C). Double peaks were found in Pcf11 intron 4 in the Inr-ahd1/+ heterozygote. This change is in the conserved splicing donor site (shaded). DNA sequences of the exon intron were shown as upper- and lowercased letters.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3362299&req=5

fig2: Lesions identified in the Pcf11 gene from the Inr-a mutations. (A) A stop codon found in the Inr-aEMS-2/+ heterozygote. A base pair of C:G was changed to T:A by EMS mutagenesis, thus changing 456R to a stop codon (Z). The double peaks indicate a nucleotide change. DNA sequence and its translation are shown. (B) A replacement of 7 bp with 5 bp (colored in DNA sequences) was found in the Inr-aγC/+ heterozygote. A series of double peaks is shown. The original and new DNA sequences and the translation of the original one are indicated. (C). Double peaks were found in Pcf11 intron 4 in the Inr-ahd1/+ heterozygote. This change is in the conserved splicing donor site (shaded). DNA sequences of the exon intron were shown as upper- and lowercased letters.
Mentions: Next, we amplified the genomic DNA and sequenced the Pcf11 gene of three Inr-a heterozygous mutants available in our lab stocks described in Materials and Methods. A stop codon mutation was found in the mutation Inr-aEMS-2, which changes 456R (according to Pcf11-PD) to a stop codon (CGA to UGA in exon 6) (Figure 2A; see Figure 1B for its location in the gene). A frame-shift mutation was found in Inr-aγC: seven base pairs (bp)(TTGCTCC) are replaced by five (GCGCA) in exon 7; thus the amino acid sequence is changed after 656 K (see Figure 2B; see Figure 1B for its location in the gene).

Bottom Line: Such effects can be reduced to the action of single genes.One gene previously found to modulate leaky alleles of the white eye color gene in Drosophila is Inverse regulator-a (Inr-a).The identification of the molecular lesion of Inr-a provides insight into the basis of this common aneuploidy effect.

View Article: PubMed Central - PubMed

Affiliation: Division of Biological Sciences, University of Missouri-Columbia, Columbia, Missouri 65211.

ABSTRACT
A common modulation of gene expression in aneuploids is an inverse correlation of the monitored gene with the dosage of another segment of the genome. Such effects can be reduced to the action of single genes. One gene previously found to modulate leaky alleles of the white eye color gene in Drosophila is Inverse regulator-a (Inr-a). Heterozygotes of mutations increase the expression of white about 2-fold, and trisomic regions surrounding the gene reduce the expression to about two-thirds of the normal diploid level. Further cytological definition of the location of this gene on the second chromosome led to a candidate pre-mRNA cleavege complex II protein (Pcf11) as the only gene in the remaining region whose mutations exhibit recessive lethality as do alleles of Inr-a. The product of Pcf11 has been implicated in transcriptional initiation, elongation, and termination reactions. Four mutant alleles showed molecular lesions predicted to lead to nonfunctional products of Pcf11. The identification of the molecular lesion of Inr-a provides insight into the basis of this common aneuploidy effect.

No MeSH data available.