Mobile Element 297 in the Abd-B gene of Drosophila melanogaster, Not Delta 88, Is Responsible for the tuh-3 Mutation

Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 679-688
Author(s):  
Judith A Mack ◽  
Ronald D Smith ◽  
David T Kuhn

The tumorous-head-3 (tuh-3) mutation has been associated with the insertion of mobile element Delta 88 at +200 on the bithorax complex (BX-C) DNA map, 5′ of all Abdominal-B (Abd-B) transcripts. Different phenotypes of tuh-3 are regulated by the tumorous-head-1 (tuh-1) maternal effect locus. In the presence of the recessive tuh-1h maternal effect, tuh-3 offspring produce homeotic abdominal and genital tissue in the head. In the presence of the dominant tuh-1g maternal effect, tuh-3 offspring have normal heads but now show genital defects. One other mutant, I127B, produces flies with identical defects to that of tuh-3 in the presence of both maternal effects. Molecular analysis of I127B revealed the insertion of mobile element 297 in the Abd-B gene, ∼25 kb downstream of the Delta 88 insertion in tuh-3. No other abnormalities were detected. Reexamination of our tuh-3 strain revealed a 297 insertion in an identical region to that of I127B, in addition to the Delta 88 insertion. Recombinants of tuh-3, carrying 297 only, produced homeotic head defects and genital defects in the presence of the tuh-1h and tuh-1R maternal effects, respectively. Recombinants of tuh-3, carrying Delta 88 only, failed to produce any defects in the presence of either maternal effect. Based upon these results, we propose that it is the 297 insertion in the Abd-B gene, not Delta 88, that is responsible for the tuh-3 mutation.

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 743-752
Author(s):  
G Packert ◽  
D T Kuhn

Abstract The tuh-1 maternal effect locus contains two naturally occurring isoalleles, tuh-1h and tuh-1g. Until recently there has been no possibility to distinguish between the tuh-1h and the tuh-1g maternal effects other than evaluating their effect on the Bithorax-Complex (BX-C) Abdominal B (Abd-B) mutant tuh-3. However, in this report we identify a bristle phenotype associated with the tuh-1 locus that has very interesting evolutionary implications. Females homozygous for tuh-1h always produce adult offspring with more bristles than females homozygous or heterozygous for tuh-1g. The effect is global. Increased bristle number occurs in the head, the thorax, and the anterior and posterior abdomen. Females totally deficient for the tuh-1 gene produce offspring with high bristle number. Thus, the bristle phenotype results from the absence of the maternally contributed tuh-1g factor. Genetic evidence shows that the bristle phenotype is caused by the tuh-1 locus and that tuh-1h is completely recessive to tuh-1g. The tuh-1 locus is located at the euchromatin-β-heterochromatin junction near the centromere of the X chromosome and deficiency analysis places the locus between the lethal genes extra organs (eo) and lethal B20 (lB20). The variance in bristle number attributable to the tuh-1 locus in nature is approximately 10.1%, an indication that the bristle phenotype is most likely a neutral, pleiotrophic side effect of tuh-1.


Genetics ◽  
1994 ◽  
Vol 137 (3) ◽  
pp. 783-789 ◽  
Author(s):  
N L Jenkins ◽  
A A Hoffmann

Abstract In Drosophila, field heritability estimates have focused on morphological traits and ignored maternal effects. This study considers heritable variation and maternal effects in a physiological trait, heat resistance. Drosophila were collected from the field in Melbourne, Australia. Resistance was determined using knock-down time at 37 degrees. Drosophila melanogaster was more resistant than Drosophila simulans, and males tended to be more resistant than females. Field heritability and maternal effects were examined in D. simulans using the regression of laboratory-reared F1 and F2 onto field-collected parents. Males from the field were crossed to a laboratory stock to obtain progeny. The additive genetic component to variation in heat resistance was large and significant, and heritability was estimated to be around 0.5. A large maternal effect was also evident. Comparisons of regression coefficients suggested that the maternal effect was not associated with cytoplasmic factors. There was no correlation between body size (as measured by wing length) and heat resistance. Unlike in the case of morphological traits, the heritability for heat resistance in nature is not less than that measured in the laboratory.


Genetics ◽  
1981 ◽  
Vol 99 (1) ◽  
pp. 99-107
Author(s):  
David T Kuhn ◽  
Daniel F Woods ◽  
Deborah J Andrew

ABSTRACT In the presence of the naturally occurring maternal-effect alleles tuh-1h or tuh-1g, the tuh-3 mutant gene can cause the tumorous-head trait or the sac-testis trait. The tuh-3 gene functions as a semidominant in the presence of the tuh-1h maternal effect. Eye-antennal structures are replaced by posterior abdominal tergites and genital structures. If tuh-1h is replaced by its naturally occurring allele tuh-1g, tuh-3 functions as a recessive hypomorph and the defect switches from anterior to posterior structures, with a male genital-disc defect appearing with variable penetrance. Function and regulation of tuh-3  + may better be understood in light of the cytological localization of tuh-3 either adjacent to or as part of the bithorax complex. The tuh-3  + gene product appears to be essential for normal development, at least in the posterior end of the embryo.


Genetics ◽  
1973 ◽  
Vol 73 (1) ◽  
pp. 73-86
Author(s):  
Arthur P Mange ◽  
L Sandler

ABSTRACT Two deficiencies for, and a dominant enhancer of, the second chromosome maternal effect mutant, "daughterless" (da), were induced with X-irradiation. Their properties were studied with respect to both da and the linked maternal effect mutant, "abnormal oocyte" (abo), with the following conclusions. (1) The most probable map positions of da and abo are: J–½–da–2½–abo, where J is a dominant marker located at 41 on the standard map. (2) The da locus is in bands 31CD-F on the polytene chromosome map; abo is to the right of 32A. (3) Because homozygous da individuals survive while individuals carrying da and a deficiency for da are lethal, it is concluded that da is hypomorphic. (4) From a weak da-like maternal effect in heterozygous da females induced by an "Enhancer of da," we have confirmed a previous report that (a) the amount of sex chromosome heterochromatin contributed by the father can influence the severity of the da maternal effect, and (b) the sex chromosome heterochromatin which influences the da effect is different from that which influences the abo effect. (5) The possibility that da and abo are in a special region of chromosome 2 concerned with the regulation of sex chromosome heterochromatin is strengthened by the observation that the Enhancer of da appears to rescue abnormal eggs produced by homozygous abo mothers. (6) The Enhancer of da is a translocation between chromosomes 2 and 3 with the second chromosome breakpoint in the basal heterochromatin; because the enhancing effect maps in this region of chromosome 2, it is possible that autosomal, as well as sex chromosomal, heterochromatin interacts with da and abo.


Gene ◽  
2000 ◽  
Vol 246 (1-2) ◽  
pp. 157-167 ◽  
Author(s):  
Thorsten Burmester ◽  
Mátyás Mink ◽  
Margit Pál ◽  
Zsolt Lászlóffy ◽  
Jean-Antoine Lepesant ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document