A Genetic Screen for Zygotic Embryonic Lethal Mutations Affecting Cuticular Morphology in the Wasp Nasonia vitripennis

Genetics ◽  
2000 ◽  
Vol 154 (3) ◽  
pp. 1213-1229
Author(s):  
Mary Anne Pultz ◽  
Kristin K Zimmerman ◽  
Neal M Alto ◽  
Matt Kaeberlein ◽  
Sarah K Lange ◽  
...  
Keyword(s):  
Regulatory Gene ◽  
Polycomb Group ◽  
Embryonic Patterning ◽  
Nasonia Vitripennis ◽  
Entire Genome ◽  
Anteroposterior Patterning ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
Mutant Phenotypes

Abstract We have screened for zygotic embryonic lethal mutations affecting cuticular morphology in Nasonia vitripennis (Hymenoptera; Chalcidoidea). Our broad goal was to investigate the use of Nasonia for genetically surveying conservation and change in regulatory gene systems, as a means to understand the diversity of developmental strategies that have arisen during the course of evolution. Specifically, we aim to compare anteroposterior patterning gene functions in two long germ band insects, Nasonia and Drosophila. In Nasonia, unfertilized eggs develop as haploid males while fertilized eggs develop as diploid females, so the entire genome can be screened for recessive zygotic mutations by examining the progeny of F1 females. We describe 74 of >100 lines with embryonic cuticular mutant phenotypes, including representatives of coordinate, gap, pair-rule, segment polarity, homeotic, and Polycomb group functions, as well as mutants with novel phenotypes not directly comparable to those of known Drosophila genes. We conclude that Nasonia is a tractable experimental organism for comparative developmental genetic study. The mutants isolated here have begun to outline the extent of conservation and change in the genetic programs controlling embryonic patterning in Nasonia and Drosophila.

Maternal-effect lethal mutations on linkage group II of Caenorhabditis elegans.

Genetics ◽  
1988 ◽  
Vol 120 (4) ◽  
pp. 977-986
Author(s):  
K J Kemphues ◽  
M Kusch ◽  
N Wolf
Keyword(s):  
Caenorhabditis Elegans ◽  
Linkage Group ◽  
Maternal Effect ◽  
Essential Genes ◽  
The Other ◽  
C Elegans ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
F1 Progeny

Abstract We have analyzed a set of linkage group (LG) II maternal-effect lethal mutations in Caenorhabditis elegans isolated by a new screening procedure. Screens of 12,455 F1 progeny from mutagenized adults resulted in the recovery of 54 maternal-effect lethal mutations identifying 29 genes. Of the 54 mutations, 39 are strict maternal-effect mutations defining 17 genes. These 17 genes fall into two classes distinguished by frequency of mutation to strict maternal-effect lethality. The smaller class, comprised of four genes, mutated to strict maternal-effect lethality at a frequency close to 5 X 10(-4), a rate typical of essential genes in C. elegans. Two of these genes are expressed during oogenesis and required exclusively for embryogenesis (pure maternal genes), one appears to be required specifically for meiosis, and the fourth has a more complex pattern of expression. The other 13 genes were represented by only one or two strict maternal alleles each. Two of these are identical genes previously identified by nonmaternal embryonic lethal mutations. We interpret our results to mean that although many C. elegans genes can mutate to strict maternal-effect lethality, most genes mutate to that phenotype rarely. Pure maternal genes, however, are among a smaller class of genes that mutate to maternal-effect lethality at typical rates. If our interpretation is correct, we are near saturation for pure maternal genes in the region of LG II balanced by mnC1. We conclude that the number of pure maternal genes in C. elegans is small, being probably not much higher than 12.

Extensive zygotic control of the anteroposterior axis in the wasp Nasonia vitripennis

Development ◽  
1999 ◽  
Vol 126 (4) ◽  
pp. 701-710 ◽  
Author(s):  
M.A. Pultz ◽  
J.N. Pitt ◽  
N.M. Alto
Keyword(s):  
Parasitoid Wasp ◽  
Axis Formation ◽  
Gene Products ◽  
Nasonia Vitripennis ◽  
Anteroposterior Patterning ◽  
Lethal Mutations ◽  
Gap Genes ◽  
Maternal Gene ◽  
Zygotic Control ◽  
Zygotic Genome

Insect axis formation is best understood in Drosophila melanogaster, where rapid anteroposterior patterning of zygotic determinants is directed by maternal gene products. The earliest zygotic control is by gap genes, which determine regions of several contiguous segments and are largely conserved in insects. We have asked genetically whether early zygotic patterning genes control similar anteroposterior domains in the parasitoid wasp Nasonia vitripennis as in Drosophila. Nasonia is advantageous for identifying and studying recessive zygotic lethal mutations because unfertilized eggs develop as males while fertilized eggs develop as females. Here we describe recessive zygotic mutations identifying three Nasonia genes: head only mutant embryos have posterior defects, resembling loss of both maternal and zygotic Drosophila caudal function; headless mutant embryos have anterior and posterior gap defects, resembling loss of both maternal and zygotic Drosophila hunchback function; squiggy mutant embryos develop only four full trunk segments, a phenotype more severe than those caused by lack of Drosophila maternal or zygotic terminal gene functions. These results indicate greater dependence on the zygotic genome to control early patterning in Nasonia than in the fly.

scholarly journals Three ENU-induced alleles of the murine quaking locus are recessive embryonic lethal mutations

1988 ◽  
Vol 51 (2) ◽  
pp. 95-102 ◽  
Author(s):  
Monica J. Justice ◽  
Vernon C. Bode
Keyword(s):  
Mouse Chromosome ◽  
Lethal Mutation ◽  
Chromosome 17 ◽  
Wild Type ◽  
Embryonic Survival ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
Precise Time ◽  
New Alleles

SummaryThe quaking (qk) locus on mouse chromosome 17 has been defined by a single viable quaking allele. Three new alleles of quaking were selected after ENU mutagenesis by their failure to complement the quaking phenotype. The qkk2 allele was induced on wild-type chromatin and the qkkt1 and qkkt4 alleles were induced on t-chromatin. Each is a recessive embryonic lethal mutation. They fail to complement each other and are not complemented by the deletion, TtOrl. Homozygotes and hemizygotes die at 8–9·5 days gestation, but not at a single precise time. Because the classical quaking mutation complements the lethality of these new alleles, but they fail to complement its quaking phenotype (myelination defect), we conclude that the quaking+ function is required for embryonic survival as well as for myelination.

scholarly journals Induction of recessive lethal and specific locus mutations in the zebrafish with ethyl nitrosourea

1992 ◽  
Vol 59 (2) ◽  
pp. 103-116 ◽  
Author(s):  
David Jonah Grunwald ◽  
George Streisinger
Keyword(s):  
Zebrafish Embryo ◽  
Germ Line ◽  
Point Mutations ◽  
Mature Sperm ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
Sperm Dna ◽  
Specific Locus

SummaryRecessive lethal mutations and mutations at the gol-1 locus were induced in the zebrafish by exposure of mature sperm to the alkylating agent ethyl nitrosourea (ENU). Embryonic lethal phenotypes were recognized among the parthenogenetic progeny of mutagenized animals or among the progeny of daughters of mutagenized animals. Novel specific locus mutations were identified by the failure of mutagenized chromosomes to complement pre-existing mutant alleles at the gol-1 locus. Each mutagenized individual harboured approximately 10 embryonic lethal mutations in its germ line and about 1 in 500 mutagenized animals harboured a new mutation at the gol-1 locus. Three lines of evidence indicate that the majority of mutations that were recovered following treatment of mature sperm with ENU were probably point mutations. First, the soma and germ lines of mutagenized animals were mosaic, as expected following simple alkylation of sperm DNA. Second, mutations induced by ENU at the gol-1 locus affected pigmentation but not viability, unlike the majority of mutations induced at this locus with y-irradiation. Third, the ratio of specific locus: recessive lethal mutations induced by ENU was approximately 50-fold lower than the ratio observed following mutagenesis with y-rays. Comparison of the incidence with which embryonic recessive lethal mutations were induced with the incidence with which specific locus mutations arose indicates that there are greater than 5000 genes essential to the development and viability of the zebrafish embryo.

scholarly journals A Survey of New Temperature-Sensitive, Embryonic-Lethal Mutations in C. elegans: 24 Alleles of Thirteen Genes

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e16644 ◽  
Author(s):  
Sean M. O'Rourke ◽  
Clayton Carter ◽  
Luke Carter ◽  
Sara N. Christensen ◽  
Minh P. Jones ◽  
...  
Keyword(s):  
Temperature Sensitive ◽  
C Elegans ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations

scholarly journals NGS-based reverse genetic screen for common embryonic lethal mutations compromising fertility in livestock

2016 ◽  
Vol 26 (10) ◽  
pp. 1333-1341 ◽  
Author(s):  
Carole Charlier ◽  
Wanbo Li ◽  
Chad Harland ◽  
Mathew Littlejohn ◽  
Wouter Coppieters ◽  
...  
Keyword(s):  
Genetic Screen ◽  
Reverse Genetic ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
Reverse Genetic Screen

MUTATION BREEDING AND THE MUTANT SECTOR PROBLEM IN ARABIDOPSIS

1974 ◽  
Vol 16 (2) ◽  
pp. 476-480 ◽  
Author(s):  
J. R. Harle
Keyword(s):  
Prolonged Exposure ◽  
Germ Line ◽  
Mutation Breeding ◽  
Experimental Plant ◽  
Lethal Mutations ◽  
Embryonic Lethal ◽  
Embryonic Lethal Mutations ◽  
Segregation Ratios ◽  
The Difference ◽  
Germinating Seeds

In reply to the objections raised by Redei (1974), the 34:1 segregation ratios of Harle (1972), which had been interpreted as indicating a "germ line" consisting of 8 or 9 cells in the resting Arabidopsis seed, were reexamined in comparison with the 7:1 ratios and 1 or 2 cells found by other workers. The difference was not caused by prolonged exposure of successive cell generations, as the first cell division in germinating seeds occurred only after 39 hours, while the half life for the decomposition of the mutagen (diethyl sulfate) was one hour. The new method for calculating mutation frequencies also did not account for the difference, as the use of the standard method produced almost the same conclusions. The difference found could be ascribed to the use of viable mutations in the calculations, rather than the chlorophyl-deficient and embryonic-lethal mutations normally used in experimental plant mutagenesis. The suggested modification of mutation breeding procedures was reaffirmed.

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