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MEIOSIS IN MALE DROSOPHILA MELANOGASTER I. ISOLATION AND CHARACTERIZATION OF MEIOTIC MUTANTS AFFECTING SECOND CHROMOSOME DISJUNCTION
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ABSTRACT
Two second chromosome, EMS-induced, meiotic mutants which cause an increase in second chromosome nondisjunction are described. The first mutant is recessive and causes an increase in second chromosome nondisjunction in both males and females. It causes no increase in nondisjunction of the sex chromosomes in either sex, nor of the third chromosome in females. No haplo-4-progeny were recovered from either sex. Thus, it appears that this mutant, which is localized to the second chromosome, affects only second chromosome disjunction and acts in both sexes.—The other mutant affects chromosome disjunction in males and has no effect in females. Nondisjunction occurs at the first meiotic division. Sex chromosome disjunction in the presence of this mutant is similar to that of sc4sc8, with an excess of X and nullo-XY sperm relative to Y and XY sperm. In some lines, there is an excess of nullo-2 sperm relative to diplo-2 sperm, which appears to be regulated, in part, by the Y chromosome. A normal Y chromosome causes an increase in nullo-2 sperm, where BsY does not. There is also a high correlation between second and sex chromosome nondisjunction. Nearly half of the second chromosome exceptions are also nondisjunctional for the sex chromosomes. Among the double exceptions, there is an excess of XY nullo-2 and nullo-XY diplo-2 gametes. Meiotic drive, chromosome loss and nonhomologous pairing are considered as possible explanations for the double exceptions.
Title: MEIOSIS IN MALE DROSOPHILA MELANOGASTER I. ISOLATION AND CHARACTERIZATION OF MEIOTIC MUTANTS AFFECTING SECOND CHROMOSOME DISJUNCTION
Description:
ABSTRACT
Two second chromosome, EMS-induced, meiotic mutants which cause an increase in second chromosome nondisjunction are described.
The first mutant is recessive and causes an increase in second chromosome nondisjunction in both males and females.
It causes no increase in nondisjunction of the sex chromosomes in either sex, nor of the third chromosome in females.
No haplo-4-progeny were recovered from either sex.
Thus, it appears that this mutant, which is localized to the second chromosome, affects only second chromosome disjunction and acts in both sexes.
—The other mutant affects chromosome disjunction in males and has no effect in females.
Nondisjunction occurs at the first meiotic division.
Sex chromosome disjunction in the presence of this mutant is similar to that of sc4sc8, with an excess of X and nullo-XY sperm relative to Y and XY sperm.
In some lines, there is an excess of nullo-2 sperm relative to diplo-2 sperm, which appears to be regulated, in part, by the Y chromosome.
A normal Y chromosome causes an increase in nullo-2 sperm, where BsY does not.
There is also a high correlation between second and sex chromosome nondisjunction.
Nearly half of the second chromosome exceptions are also nondisjunctional for the sex chromosomes.
Among the double exceptions, there is an excess of XY nullo-2 and nullo-XY diplo-2 gametes.
Meiotic drive, chromosome loss and nonhomologous pairing are considered as possible explanations for the double exceptions.
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