Structures of spontaneous deletions in Caenorhabditis elegans

1988 ◽  
Vol 8 (9) ◽  
pp. 3748-3754
Author(s):  
R A Pulak ◽  
P Anderson
Keyword(s):  
Caenorhabditis Elegans ◽  
Structural Features ◽  
Chain Gene ◽  
Wild Type ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Base Pairs ◽  
Average Size ◽  
Distinguishing Features ◽  
Small Average Size

We have investigated the structural features of spontaneous deletions in Caenorhabditis elegans. We cloned and sequenced the junctions of 16 spontaneous deletions affecting the unc-54 myosin heavy-chain gene and compared their sequences with those of the wild type. We analyzed these sequences in an attempt to identify structural features of the gene that are consistently involved in the spontaneous deletion process. Most deletions (15 of 16) removed a single contiguous region of DNA, with no nucleotides inserted or rearranged at the deletion junctions; one deletion was more complex. unc-54 deletions were small, averaging 600 base pairs in length, and were randomly distributed throughout the gene. Unlike deletions that occur in Escherichia coli, spontaneous unc-54 deletions did not contain statistically significant direct or inverted repeats at or near their termini. Except for their small average size, we have not identified any distinguishing features of their sequence or structure. We discuss these results with regard to the mechanisms for spontaneous deletion in eucaryotic and procaryotic cells.

scholarly journals Structures of spontaneous deletions in Caenorhabditis elegans.

1988 ◽  
Vol 8 (9) ◽  
pp. 3748-3754 ◽  
Author(s):  
R A Pulak ◽  
P Anderson
Keyword(s):  
Caenorhabditis Elegans ◽  
Structural Features ◽  
Chain Gene ◽  
Wild Type ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Base Pairs ◽  
Average Size ◽  
Distinguishing Features ◽  
Small Average Size

We have investigated the structural features of spontaneous deletions in Caenorhabditis elegans. We cloned and sequenced the junctions of 16 spontaneous deletions affecting the unc-54 myosin heavy-chain gene and compared their sequences with those of the wild type. We analyzed these sequences in an attempt to identify structural features of the gene that are consistently involved in the spontaneous deletion process. Most deletions (15 of 16) removed a single contiguous region of DNA, with no nucleotides inserted or rearranged at the deletion junctions; one deletion was more complex. unc-54 deletions were small, averaging 600 base pairs in length, and were randomly distributed throughout the gene. Unlike deletions that occur in Escherichia coli, spontaneous unc-54 deletions did not contain statistically significant direct or inverted repeats at or near their termini. Except for their small average size, we have not identified any distinguishing features of their sequence or structure. We discuss these results with regard to the mechanisms for spontaneous deletion in eucaryotic and procaryotic cells.

scholarly journals THE GENE STRUCTURES OF SPONTANEOUS MUTATIONS AFFECTING A CAENORHABDITIS ELEGANS MYOSIN HEAVY CHAIN GENE

Genetics ◽  
1985 ◽  
Vol 109 (1) ◽  
pp. 67-79
Author(s):  
David Eide ◽  
Philip Anderson
Keyword(s):  
Caenorhabditis Elegans ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Chain Gene ◽  
Spontaneous Mutations ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Base Pairs ◽  
C Elegans ◽  
Gene Structures

ABSTRACT We have isolated spontaneous mutations affecting the unc-54 major myosin heavy chain gene of Caenorhabditis elegans (variety Bristol). Spontaneous unc-54 mutants occur in C. elegans populations at a frequency of approximately 3 × 10-7. We have studied the gene structure of 65 independent unc-54 mutations using filter-transfer hybridization techniques. Most unc-54 mutations (50 of 65) exhibit no abnormalities detected with these techniques; these mutations are small lesions affecting less than 100 base pairs. Approximately 17% of the mutations (11 of 65) are simple deletions, ranging in size from less than 100 base pairs to greater than 17 kilobases. One isolate contains two separate deletions, each of which affects unc-54. Two mutants contain tandem genetic duplications that include a portion of unc-54 and extend 8-10 kilobases beyond the 5' terminus of the mRNA. Conspicuously absent from our collection of spontaneous unc-54 mutations are any resulting from insertion of transposable genetic elements. Such mutants, if they occur, must arise at a frequency of less than 5 × 10-9

scholarly journals Splicing removes the Caenorhabditis elegans transposon Tc1 from most mutant pre-mRNAs.

1996 ◽  
Vol 16 (1) ◽  
pp. 422-429 ◽  
Author(s):  
A M Rushforth ◽  
P Anderson
Keyword(s):  
Caenorhabditis Elegans ◽  
Negative Selection ◽  
Target Gene ◽  
Mrna Processing ◽  
Chain Gene ◽  
Splice Sites ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Mature Mrna

The transposable element Tc1 is responsible for most spontaneous mutations that occur in many Caenorhabditis elegans strains. We analyzed the abundance and sequence of mRNAs expressed from five different Tc1 insertions within either hlh-1 (a MyoD homolog) or unc-54 (a myosin heavy chain gene). Each of the mutants expresses substantial quantities of mature mRNA in which most or all of Tc1 has been removed by splicing. Such mRNAs contain small insertions of Tc1 sequences and/or deletions of target gene sequences at the resulting spliced junctions. Most of these mutant mRNAs do not contain premature stop codons, and many are translated in frame to produce proteins that are functional in vivo. The number and variety of splice sites used to remove Tc1 from these mutant pre-mRNAs are remarkable. Two-thirds of the Tc1-containing introns removed from hlh-1 and unc-54 lack either the 5'-GU or AG-3' dinucleotides typically found at the termini of eukaryotic introns. We conclude that splicing to remove Tc1 from mutant pre-mRNAs allows many Tc1 insertions to be phenotypically silent. Such mRNA processing may help Tc1 escape negative selection.

scholarly journals A SECOND INFORMATIONAL SUPPRESSOR, SUP-7 X, IN CAENORHABDITIS ELEGANS

Genetics ◽  
1981 ◽  
Vol 97 (2) ◽  
pp. 307-325
Author(s):  
Robert H Waterston
Keyword(s):  
Suppressor Gene ◽  
Null Alleles ◽  
Chain Gene ◽  
Wild Type ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
C Elegans ◽  
X Linkage ◽  
Suppressor Mutations ◽  
Dose Dependent

ABSTRACT More than 30 independent suppressor mutations have been obtained in the nematode C. elegans through reversion analysis of two unc-13 mutants. Many of the new isolates map to the region of the previously identified informational suppressor, sup-5 III (Waterston and Brenner 1978). Several of the other suppressor mutations map to the left half of the X-linkage group and define a second suppressor gene, sup-7 X. In tests against 40 mutations in six genes, the sup-7(st5) allele was found to suppress to a greater extent the same alleles acted on by sup-5(e1464). Like sup-5(e1464), sup-7(st5) acts on null alleles of the myosin heavy-chain gene unc-54 I (MacLeod et al. 1977; MacLeod, Waterston and Brenner 1977) and the putative paramyosin gene unc-15 I (Waterston et al. 1977). Chemical analysis of unc-15(e1214); sup-7(st5) animals show that paramyosin is restored to more than 30% of the wild-type level. —As was observed for sup-5(e1464), suppression by sup-7(st5) is dose dependent and is greater in animals grown at 15° than at 25°. However, associated with this increased suppression is a decreased viability of sup-7(st5) homozygotes. Reversion of the lethality has resulted in the isolation of deficiency mutations that complement st5 lethality, but lack suppressor function. These properties of sup-7(st5) suggest that it, like sup-5(e1464), is an informational suppressor of null alleles, and its reversion via deficiencies further narrows the possible explanations of its action.

Mutations in the unc-54 myosin heavy chain gene of caenorhabditis elegans that alter contractility but not muscle structure

Cell ◽  
1982 ◽  
Vol 29 (3) ◽  
pp. 773-781 ◽  
Author(s):  
Donald G. Moerman ◽  
Santiago Plurad ◽  
Robert H. Waterston ◽  
David L. Baillie
Keyword(s):  
Caenorhabditis Elegans ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Muscle Structure

scholarly journals Transformation of Drosophila melanogaster with the wild-type myosin heavy-chain gene: rescue of mutant phenotypes and analysis of defects caused by overexpression.

1994 ◽  
Vol 126 (3) ◽  
pp. 689-699 ◽  
Author(s):  
R M Cripps ◽  
K D Becker ◽  
M Mardahl ◽  
W A Kronert ◽  
D Hodges ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Copy Number ◽  
Chain Gene ◽  
Wild Type ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene ◽  
Flight Muscles ◽  
Mutant Phenotypes

We have transformed Drosophila melanogaster with a genomic construct containing the entire wild-type myosin heavy-chain gene, Mhc, together with approximately 9 kb of flanking DNA on each side. Three independent lines stably express myosin heavy-chain protein (MHC) at approximately wild-type levels. The MHC produced is functional since it rescues the mutant phenotypes of a number of different Mhc alleles: the amorphic allele Mhc1, the indirect flight muscle and jump muscle-specific amorphic allele Mhc10, and the hypomorphic allele Mhc2. We show that the Mhc2 mutation is due to the insertion of a transposable element in an intron of Mhc. Since a reduction in MHC in the indirect flight muscles alters the myosin/actin protein ratio and results in myofibrillar defects, we determined the effects of an increase in the effective copy number of Mhc. The presence of four copies of Mhc results in overabundance of the protein and a flightless phenotype. Electron microscopy reveals concomitant defects in the indirect flight muscles, with excess thick filaments at the periphery of the myofibrils. Further increases in copy number are lethal. These results demonstrate the usefulness and potential of the transgenic system to study myosin function in Drosophila. They also show that overexpression of wild-type protein in muscle may disrupt the function of not only the indirect flight but also other muscles of the organism.

Molecular analysis of the unc-54 myosin heavy-chain gene of Caenorhabditis elegans

Nature ◽  
1981 ◽  
Vol 291 (5814) ◽  
pp. 386-390 ◽  
Author(s):  
Alexander R. MacLeod ◽  
Jonathan Karn ◽  
Sydney Brenner
Keyword(s):  
Caenorhabditis Elegans ◽  
Myosin Heavy Chain ◽  
Molecular Analysis ◽  
Heavy Chain ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene
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