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At least 19 recordsLinked to original sources

PubMed1991

Sex-linked and maternal effects on growth in chickens.

A study was designed to estimate the contribution of various types of genetic variation in growth of chickens using populations that widely differed in growth rate. Populations tested included a commercially developed sire line (CM), a fertility-selected, broiler-type line (FS), and the pureline Jersey Giant (JG). A full set of F1 crosses and purelines of both sexes was used to estimate the following genetic effects: heterosis due to the autosomes, heterosis due to the sex chromosomes, average line effects, maternal effects, and additive sex linkage. Average line effects were highly significant beyond hatching for both body weight and shank length, with rank-order CM greater than FS, which was greater than JG. Significant differences between the sexes within a line were observed for CM and JG line effects, confirming the existence of sex-linked factors. There was no average heterosis or sex-by-heterosis interaction for growth-related traits, but specific heterosis was frequently significant. Maternal effects were sporadic and generally of little importance beyond hatching. Additive sex linkage, however, was highly significant and influenced body weight beyond hatching. These data indicate that the primary advantages in increasing growth via cross-breeding in chickens comes from average line effects and additive sex linkage. Heterosis and maternal effects can influence performance, especially in specific crosses, but these effects appear to be sporadic and of less importance than sex linkage.

Animals↗

PubMed1992

Reduced animal model with differential genetic grouping for direct and maternal effects.

Mixed-model equations for the reduced animal model with maternal effects and different genetic grouping of unknown parents for additive direct and maternal effects are derived. The matrices that relate the expected value and the variance of the breeding values of non-parents to the parents, as well as the different contributions of parental and non-parental breeding values, to the resulting mixed-model equations are presented. Mis-specification of additive maternal variance and the additive covariance between direct and maternal effects, arising from missing information on the dams of known individuals with records, is discussed. To avoid an incorrect specification of the variance-covariance matrix of the records without having to invert a nondiagonal variance of the residual terms, the breeding values of the unknown dams of individuals with records are included in the equations. Breeding values of non-parents are back-solved after the solutions for genetic groups and breeding values of parents are computed as simply as in cases in which maternal effects are absent. A numerical example is included to illustrate the derivations.

Animals↗

PubMed1990

Alternative animal models with maternal effects and foster dams.

Effects of foster dams can be included in genetic evaluations using animal models with maternal effects in several ways. The alternatives discussed involve minor changes in computing strategies from strategies used with reduced animal models that predict breeding values for direct and maternal effects. The easiest alternative is to assign foster dams to groups by breed and time period and add equations for fixed effects of breed-period. Random and, assumed, independent effects of foster dams can be nested in breed-period groups. If foster dams do not repeat, then those effects can be absorbed into equations for other fixed effects, additive direct breeding value and breed-period effects by slightly modifying least squares contributions to coefficients of those equations. A third alternative for foster dams of the same breed is to add breeding values for foster dams for direct and maternal effects to solution vectors for breeding values. Equations are similar to those without foster dams, except that least squares contributions to coefficient matrix and right-hand sides are to equations for maternal breeding values and nongenetic maternal effects of foster dams rather than biological dams. Relationships and covariance between direct and maternal effects contribute mixed-model coefficients to direct and maternal breeding value equations of biological dams. This alternative basically requires only larger solution vectors for direct and maternal breeding values to accommodate foster dams that might not be included. The fourth alternative includes a vector of maternal breeding values for foster dams of each breed of foster dams and would require using rules of Westell to calculate coefficients due to relationships and fixed maternal genetic groups within each breed of foster dam. These alternatives do not require much additional computational effort compared with full or reduced animal model equations when the transformation to predict breeding values is used with Westell's rules to calculate coefficients due to relationships and genetic group effects due to prior genetic selection.

Animals↗

PubMed1977

Maternal effects in human cleft lip and palate.

To look for a persistent maternal effect of CL(P) and CP, 8,000 pedigrees were screened for half sibships, and data were pooled from 16 investigators. After excluding known genetic or cytogenetic diagnoses from the probands with facial clefts, a recurrence risk of .011 was obtained for CL(P) based upon 342 maternal half sibs. This was nearly identical to the risk of .014 based upon 210 paternal half sibs. CP proband frequencies of .004 for maternal half sibs and .009 for the paternal counterparts were also found. The lack of significant maternal effects in this data supports previously reported data from twin studies and from interracial crosses from Hawaii. The lack of maternal effect in human CL(P) and CP is in contrast to genetic data on clefting in mice.

Cleft Lip↗

PubMed1992

Maternal-effect selfish genes in flour beetles.

A previously unknown class of dominant, maternal-effect lethal M factors was found to be widespread in natural populations of the flour beetle, Tribolium castaneum, collected on several continents. Such factors are integrated into the host chromosomes at variable locations and show the remarkable property of self-selection by maternal-effect lethality to all hatchlings that do not inherit a copy of the factor itself. Offspring are rescued by either paternally or maternally inherited copies. The M-bearing chromosome is thereby perpetuated at the expense of its non-M homolog. M factors that map to different regions of the genome do not rescue one another's maternal-effect lethality. Factors expressing these properties are predicted to spread in a population, even in the absence of any additional selective advantage. Similar factors also occur in the related species T. confusum.

Animals↗

PubMed1991

abnormal chromatin (abc), a maternal-effect locus in Drosophila melanogaster.

Mutations in the maternal-effect gene abnormal chromatin (abc) in Drosophila melanogaster result in a variety of defects involving nuclear replication/division. Three recessive alleles of this gene, which maps near 51F on chromosome 2, all result in female sterility. They cause slower embryonic development that is usually abnormal from the earliest nuclear divisions and arrested by the sixth one. Nuclei tend to be large and erratically distributed, some intensely staining. Mitotic asynchrony is common. Few embryos reach the gastrula stage and none hatch. With the weakest allele, fsPL, bridges between nuclei are common; abnormal chromatin clumps that resemble yolk nuclei occur before the other nuclei reach the surface; and spindle anomalies and DNA wads with numerous centrosomes are seen. Females with the stronger alleles, fsA5 and fs27, lay fewer eggs and a smaller proportion of embryos reach blastoderm; developmental arrest occurs earlier, usually with several large nuclei distributed along the length of the embryo. Chorion defects occur in all three mutants. Mitotic asynchrony, nuclear bridging, endoreduplication and nuclear behavior aberrant from the first division suggest that the abc gene product operates in DNA replication/nuclear division. Larval (homozygous F1) neuroblast chromosome structure and mitotic indices are normal, indicating that any mitotic function is strictly maternal, i.e. abc is not a general mitotic gene. Thus abc is one of a few known genes with a maternal effect that appears to function in the embryonic cell cycle.

Alleles↗

PubMed1990

Absorption of equations for non-parents for an animal model with maternal effects and genetic groups.

Rules for forming the mixed-model equations for the reduced animal model with all relationships and including maternal effects have been set out by Quaas and Pollak. They also have shown how to simplify the mixed-model equations when genetic group effects are included in the model with what has become known as the Q-P transformation. Westell has given rules for calculating the coefficients for the Q-P transformed equations that are associated with the inverse of the numerator relationship matrix and genetic group effects. Those rules can be extended to include maternal effects and genetic groups for maternal as well as direct effects. As with the rules of Quaas and Pollak for the equations for the reduced animal model, a similar set of rules can be obtained for the genetic groups model after the Q-P transformation. The rules are derived easily by examining the algebraic results of absorbing the direct and maternal breeding value equations for non-parents into the parent breeding value, group and fixed effects equations. These rules involve Westell's rules and the inverse elements of the genetic (co)variance matrix for direct and maternal additive genetic effects. The rules make calculation of breeding values for parents for models including direct and maternal genetic group effects nearly as easy as for models without genetic group effects. Back solution for direct and maternal breeding values of non-parents similarly is as simple as when genetic group effects are not in the model.

Animals↗

PubMed1989

Zygotic lethals with specific maternal effect phenotypes in Drosophila melanogaster. I. Loci on the X chromosome.

In order to identify all X-linked zygotic lethal loci that exhibit a specific maternal effect on embryonic development, germline clonal analyses of X-linked zygotic lethal mutations have been performed. Two strategies were employed. In Screen A germline clonal analysis of 441 mutations at 211 previously mapped X-linked loci within defined regions was performed. In Screen B germline clonal analysis of 581 larval and pupal mutations distributed throughout the entire length of the X chromosome was performed. These approaches provide an 86% level of saturation for X-linked late zygotic lethals (larval and pupal) with specific maternal effect embryonic lethal phenotypes. The maternal effect phenotypes of these mutations are described.

Animals↗

PubMed1990

Genetics of 51D-52A, a region containing several maternal-effect genes and two maternal-specific transcripts in Drosophila.

Two genomic clones exhibiting a maternal-specific pattern of expression map to cytological region 52A. To elucidate the function of these clones we have undertaken a mutagenesis of the cytological region 51D-52A. This paper presents the results of this screen and the preliminary analysis of female-sterile and lethal mutations isolated. A total of twelve complementation groups have been identified, four of which are defined exclusively by female-sterile alleles. Only one visible mutation was isolated, a recessive temperature-sensitive allele of Thickened-arista (Tarts). Several of the seven lethal loci display an embryonic lethal phase. Three of the four female-sterile loci affect chorion structure with one resulting in underamplification of the chorion genes, and two (possibly three) of the four female-steriles affect nuclear division/DNA replication. Thus it appears that this is a "developmentally important" region, possibly representing a clustering of genes involved in either DNA replication or nuclear division.

Alleles↗

PubMed1991

Rescue from the abnormal oocyte maternal-effect lethality by ABO heterochromatin in Drosophila melanogaster.

The euchromatic maternal-effect mutation abnormal oocyte (abo), of Drosophila melanogaster interacts with regions of heterochromatin known as ABO, which reside on the X, Y and second chromosomes. Here, we show that survival of progeny from abo females depends in part upon the maternal dosage of ABO heterochromatin. A comparison was made of the recovery of genotypically identical progeny from abo mothers bearing sex chromosomes of various ABO contents. The results show that the recovery of daughters was decreased if mothers were ABO-/ABO-. However, no decrease was observed if mothers were ABO+/ABO-. In addition, the survival of daughters was greater when they received an ABO-X chromosome from an ABO-/ABO+ mother rather than the father. We suggest that these results reflect a complementation or interaction between the ABO-deficient X and the ABO heterochromatin in the maternal genome. This proposed interaction could occur early in oogenesis in the mother or prior to completion of meiosis I in the fertilized egg. To determine if zygotic dosage of ABO heterochromatin might also be important at very early stages of embryogenesis, we examined the timing of zygotic rescue by paternally donated ABO heterochromatin using a second mutation, paternal loss (pal). Homozygous pal males produce progeny which lose paternally derived chromosomes during the early zygotic divisions. Zygotes that have lost a paternal sex chromosome in a fraction of their nuclei will be mosaic for the amount of ABO heterochromatin. By monitoring the recovery of pal-induced mosaics from abo and abo+ females, we could determine the temporal and spatial requirements for ABO function. Results show that the survival of progeny from the abo maternal-effect lethality was increased if ABO heterochromatin was present prior to the pal-induced loss event. Analysis of mosaic patterns did not reveal a specific lethal focus. We conclude from these results that ABO heterochromatin serves its vital function prior to completion of the early cleavage divisions in progeny of abo mothers.

Animals↗

PubMed1989

Genetic correlations and maternal effect coefficients obtained from offspring-parent regression.

Additive genetic variances and covariances of quantitative characters are necessary to predict the evolutionary response of the mean phenotype vector in a population to natural or artificial selection. Standard formulas for estimating these parameters, from the resemblance between relatives in one or two characters at a time, are biased by natural selection on the parents and by maternal effects. We show how these biases can be removed using a multivariate analysis of offspring-parent regressions. A dynamic model of maternal effects demonstrates that, in addition to the phenotypic variance-covariance matrix of the characters, sufficient parameters for predicting the response of the mean phenotype vector to weak selection are the additive genetic variance-covariance matrix and a set of causal coefficients for maternal effects. These can be simultaneously estimated from offspring-parent regressions alone, in some cases just from the daughter-mother regressions, if all of the important selected and maternal characters have been measured and included in the analysis.

Analysis of Variance↗

PubMed1978

Genetic analysis of two allelic temperature-sensitive mutants of Drosophila melanogaster both of which are zygotic and maternal-effect lethals.

After fertilization, the development of a zygote depends upon both gene products synthesized by its maternal parent and gene products synthesized by the zygote itself. To analyze genetically the relative contributions of these two sources of gene products, several laboratories have been isolating two classes of mutants of Drosophila melanogaster: maternal-effect lethals and zygotic lethals. This report concerns the analysis of two temperature-sensitive mutants, OX736hs and PC025hs, which were isolated as alleles of a small-disc mutant, l(3)1902. These alleles are not only zygotic lethals, but also maternal-effect lethals. They have temperature-sensitive periods during larval life and during oogenesis. Mutant larvae exposed continuously to restrictive temperature have small discs. One-or two-day exposures to the restrictive temperature administered during the third larval instar lead to a homeotic transformation of the midlegs and hindlegs to the pattern characteristic of the forelegs. Mutant females exposed to the restrictive temperature during oogenesis produce eggs that can develop until gastrulation, but do not hatch.--The existence of these mutants, and one that was recently described by another group, implies that there may be a class of genes, heretofore unrecognized, whose products are synthesized during oogenesis, are essential for embryogenesis and are also synthesized during larval stages within imaginal disc cells.

Animals↗

PubMed1976

A sex-specific, temperature-sensitive maternal effect of the daughterless mutation of Drosophila melanogaster.

Every aspect of the phenotype of the daughterless (2-41.5) maternal effect mutation was found to be strongly temperature sensitive. Above 22 degrees, da/da mothers produced no daughters; however female progeny did survive the da maternal effect if the last 60 hours of oogenesis and the first three hours of embryonic development took place at 18 degrees. The females which survived under these conditions displayed morphological abnormalities in a variety of adult cuticular structures, characterisitc of cell death during development. In contrast, their male siblings were morphologically normal. Upon prolonged exposure to 29 degrees, da/da females became sterile but continued to lay eggs. Some sexually mosaic progeny from da/da mothers survived even at 25 degrees, but the distribution and development of the female tissue in these mosaics were abnormal. It is suggested that there are multiple functions of the da+ gene during oogenesis, one of which may be required specifically for the subsequent survival of female cells throughout the embryo. In addition to and distinct from its effect during oogenesis, the da mutation acted in both sexes of progeny as a recessive temperature-sensitive lethal mutation with a TSP during the first half of embryonic development.

Animals↗

PubMed1990

Dominant maternal-effect mutations causing embryonic lethality in Caenorhabditis elegans.

We undertook screens for dominant, temperature-sensitive, maternal-effect embryonic-lethal mutations of Caenorhabditis elegans as a way to identify certain classes of genes with early embryonic functions, in particular those that are members of multigene families and those that are required in two copies for normal development. The screens have identified eight mutations, representing six loci. Mutations at three of the loci result in only maternal effects on embryonic viability. Mutations at the remaining three loci cause additional nonmaternal (zygotic) effects, including recessive lethality or sterility and dominant male mating defects. Mutations at five of the loci cause visible pregastrulation defects. Three mutations appear to be allelic with a recessive mutation of let-354. Gene dosage experiments indicate that one mutation may be a loss-of-function allele at a haploin sufficient locus. The other mutations appear to result in gain-of-function "poison" gene products. Most of these become less deleterious as the relative dosage of the corresponding wild-type allele is increased; we show that relative self-progeny viabilities for the relevant hermaphrodite genotypes are generally M/+/+ greater than M/+ greater than M/M/+ greater than M/Df greater than M/M, where M represents the dominant mutant allele.

Animals↗

PubMed1975

Change in the maternal effect in Drosophila hybrids at low temperatures.

Interspecies Drosophila hybrids of the virilis group were used to study the maternal effect (expression of the recessive glossy mutation when females of D. virilis strains carrying this mutation are crossed with D. littoralis males of the wild type) at low temperatures. The maternal effect was found to be intensified by a factor of four at 17 degrees and there was also an increase in the incidence of haplo-6 individuals (95%, as against 26% at 25 degrees), apparently as a result of the increased frequency of elimination of the 6th D. littoralis chromosome during cleavage division I.

Animals↗

PubMed1989

cappuccino and spire: two unique maternal-effect loci required for both the anteroposterior and dorsoventral patterns of the Drosophila embryo.

cappuccino and spire are unique Drosophila maternal-effect loci that participate in pattern formation in both the anteroposterior and dorsoventral axes of the early embryo. Mutant females produce embryos lacking pole cells, polar granules, and normal abdominal segmentation. They share these defects with the posterior group of maternal-effect genes. Although embryos are defective in abdominal segmentation, in double mutant combinations with Bicaudal D, abdominal segments can be formed in the anterior half of the egg. This indicates that embryos produced by mutant females contain the 'posterior determinant' required for abdominal segmentation (Nüsslein-Volhard et al. 1987) and suggests that the wild-type gene products are not required for production of the posterior determinant but, rather, for its localization or stabilization. The vasa protein, a component of polar granules, is not localized at the posterior pole of mutant egg chambers or embryos, providing additional support for the hypothesis that localization to or stabilization of substances at the posterior pole of the egg chamber is defective in mutant females. Females mutant for the strongest alleles also produce dorsalized embryos. Phenotypic analysis reveals that these dorsalized embryos also have abdominal segmentation defects. The mutant phenotypes can be ordered in a series of increasing severity. Pole cell formation is most sensitive to loss of functional gene products, followed by abdominal segmentation, whereas normal dorsoventral patterning is the least sensitive to loss of functional gene products. In addition, mutant females contain egg chambers that appear to be dorsalized, resulting in the production of eggs with dorsalized eggshells. Germ-line mosaics indicate that cappuccino and spire are required in the oocyte-nurse cell complex. This suggests that the eggshell phenotype results from altered pattern in the underlying germ cell. Also, we defined the epistatic relationships between several early patterning loci, on the basis of an analysis of the eggs and embryos produced by females doubly mutant for cappuccino or spire and other loci that affect the pattern of both the egg and the embryo. On the basis of our current knowledge of the genes involved in this process, we formulated a working model for the early steps in dorsoventral patterning.

Animals↗

PubMed1989

The Drosophila fsh locus, a maternal effect homeotic gene, encodes apparent membrane proteins.

The maternal effect gene fsh is involved in the establishment of segments and the specification of their identities; the progeny of mutant females are missing portions of thoracic and abdominal segments, and may have homeotic transformations of third thoracic segments to second thoracic segments. The fsh locus interacts synergistically with loci such as Ubx and trx in the production of homeotic transformations. We have characterized cDNA clones corresponding to the major fsh transcripts expressed in ovaries and early embryos, and to a pupal transcript. The expression of fsh transcripts in ovaries is restricted to the germline; in developing embryos, transcripts are found throughout the cytoplasm. The different ovarian/embryonic transcripts (7.6 and 5.9 kb) are generated by use of alternative polyadenylation and splice sites. These transcripts encode two large predicted proteins of 110 and 205 kDa that have unusual amino acid compositions: 40% of the residues are glycine, alanine, or serine, and there are several regions of homopolymers and simple sequence repeats. Hydropathy analysis indicates that these proteins span the membrane. We suggest that the expression of fsh proteins in the membrane of the embryo is required for proper functioning of genes such as Ubx in the specification of segmental identity.

Amino Acid Sequence↗

PubMed1989

Analysis of maternal effect mutant combinations elucidates regulation and function of the overlap of hunchback and Krüppel gene expression in the Drosophila blastoderm embryo.

The metameric organisation of the Drosophila embryo is generated early during development, due to the action of maternal effect and zygotic segmentation and homeotic genes. The gap genes participate in the complex process of pattern formation by providing a link between the maternal and the zygotic gene activities. Under the influence of maternal gene products they become expressed in distinct domains along the anteroposterior axis of the embryo; negative interactions between neighboring gap genes are thought to be involved in establishing the expression domains. The gap gene activities in turn are required for the correct patterning of the pair-rule genes; little is known, however, about the underlying mechanisms. We have monitored the distribution of gap and pair-rule genes in wild-type embryos and in embryos in which the anteroposterior body pattern is greatly simplified due to combinations of maternal effect mutations (staufen exuperantia, vasa exuperantia, vasa exuperantia, bicoid oskar, bicoid oskar torsolike, vasa torso exuperantia). We show that the domains of protein distribution of the gap genes hunchback and Krüppel overlap in wild-type embryos. Based on the analysis of the maternal mutant combinations, we suggest an explanation of how this overlap is generated. Furthermore, our data show that different constellations of gap gene activities provide different input for the pair-rule genes, and thus strongly suggest that the overlap of hunchback and Krüppel in wild-type is functional in the formation of the patterns of pair-rule genes.

Animals↗