Genetic variability of the tumorous-head maternal effect in Drosophila melanogaster

1980 ◽  
Vol 178 (2) ◽  
pp. 423-427 ◽  
Author(s):  
Charles M. Woolf ◽  
Merry B. Passage
2012 ◽  
Vol 94 (1) ◽  
pp. 1-7 ◽  
Author(s):  
PIERRE R. GÉRARD ◽  
DAVEN C. PRESGRAVES

SummaryIntrinsic postzygotic reproductive isolation is thought to result from the substitution of multiple harmless or beneficial genetic differences between species that are incidentally deleterious when combined in species hybrids, causing hybrid sterility or inviability. Genetic variability for hybrid sterility or inviability phenotypes is, however, rarely assessed in natural populations. Here, we assess variation for Drosophila simulans-encoded maternal factor(s) that cause lethality in D. simulans–Drosophila melanogaster F1 hybrid females. First, we survey genetic variability in the strength of D. simulans-mediated maternal effect hybrid lethality among 37 geographic and laboratory isolates. We find abundant variability in the strength of maternal effect hybrid lethality, ranging from complete lethality to none. Second, we assess maternal effect hybrid lethality for a subset of wild isolates made heterozygous with two so-called hybrid rescue strains. The results suggest that the D. simulans maternal effect hybrid lethality involves a diversity of alleles and/or multiple loci.


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.


2000 ◽  
Vol 222 (2) ◽  
pp. 392-404 ◽  
Author(s):  
Benjamin Loppin ◽  
Mylène Docquier ◽  
François Bonneton ◽  
Pierre Couble

1994 ◽  
Vol 48 (2) ◽  
pp. 425-434 ◽  
Author(s):  
Michael G. Ritchie ◽  
Charalambos P. Kyriacou

2008 ◽  
Vol 90 (3) ◽  
pp. 253-258 ◽  
Author(s):  
ERIC W. CROSS ◽  
MICHAEL J. SIMMONS

SummaryMutations in the RNA interference (RNAi) genes aubergine (aub), homeless and piwi were tested for effects on the frequency, distribution and coincidence of meiotic crossovers in the long arm of the X chromosome. Some increases in crossover frequency were seen in these tests, but they may have been due to a maternal effect of the balancer chromosomes that were used to maintain the RNAi mutations in stocks rather than to the RNAi mutations themselves. These same balancers produced strong zygotic interchromosomal effects when tested separately. Mutations in aub and piwi did not affect the frequency of crossing over in the centric heterochromatin of chromosome II; nor did a balancer chromosome III.


Science ◽  
1960 ◽  
Vol 132 (3440) ◽  
pp. 1652-1652
Author(s):  
J. Bennett ◽  
R. L. Capek ◽  
T. R. Kallstedt ◽  
R. E. Moisand ◽  
R. Milkman

Sign in / Sign up

Export Citation Format

Share Document