scholarly journals NON-MENDELIAN FEMALE STERILITY IN DROSOPHILA MELANOGASTER: HEREDITARY TRANSMISSION OF I FACTOR

Genetics ◽  
1976 ◽  
Vol 83 (1) ◽  
pp. 107-123
Author(s):  
G Picard

ABSTRACT Systematic crosses between various strains of Drosophila melanogaster lead in some cases to partly sterile F1 females. Two main classes of strains, inducer and reactive, may be recognized on the basis of the fertility of F1 female progeny. Females which may show incomplete sterility (SF ♀) arise only when reactive females are crossed with inducer males, other crosses, including the reciprocal, producing only fertile F1 females. SF sterility appears as the result of an interaction between two factors, R brought into the initial cross by the reactive mother and maternally inherited, and I brought by the inducer father. The present paper reports on the hereditary transmission of I factor. It is shown that when transmitted through heterozygous males, bearing chromosomes of both inducer and reactive origin, I factor may be strictly linked to any one of the three major chromosomes of inducer strains. Such chromosomes carrying I factor were called inducer chromosomes. When transmitted through heterozygous females, this Mendelian behavior fails to hold, and non-inducer chromosomes coming from reactive strains may become inducer independently of the production of recombined gametes. This phenomenon was called chromosomal contamination. This contamination occurs even between nonhomologous chromosomes.

Genetics ◽  
1979 ◽  
Vol 91 (3) ◽  
pp. 455-471
Author(s):  
Georges Picard

ABSTRACT Strains of Drosophila melanogaster can be divided into two main classes, inducer and reactive, in relation to non-Mendelian female sterility. The genetic element responsible for the inducer condition (I factor) is chromosomal and may be linked to any inducer-strain chromosome. Each chromosome carrying the I factor (i  + chromosome) can produce females showing more-or-less reduced fertility when it is introduced by paternal gametes into a reactive oocyte. As long as i+ chromosomes are transmitted through heterozygous males with reactive originating chromosomes (r chromosomes), I factor strictly follows Mendelian segregation. In contrast, in heterozygous i+/r females, a varying proportion of r chromosomes may acquire I factor independently of classical genetic recombination, by a process called chromosomal contamination. This paper reports investigation of the characteristics of the three kinds of chromosomes produced by females in which contamination occurs. It appears that the contaminated reactive chromosomes have irreversibly acquired I factor and behave like i  + chromosomes, while the i  + chromosomes used as contaminating elements and the reactive originating chromosomes that have not been contaminated have not undergone any change.


Genetics ◽  
1979 ◽  
Vol 91 (3) ◽  
pp. 473-489
Author(s):  
Georges Picard ◽  
Alain Pelisson

ABSTRACT In relation to non-Mendelian female sterility, Drosophila melanogaster strains can be divided into two main classes, inducer and reactive. The genetic element responsible for the inducer condition (I factor) is chromosomal and may be linked to any inducer-strain chromosome. Each chromosome carrying the I factor (i  + chromosome) can, when introduced by the paternal gamete into a reactive oocyte, give rise to females (denoted SF) showing more-or-less reduced fertility. As long as i  + chromosomes are transmitted through heterozygous males with reactive originating chromosomes (r chromosomes), I factor follows Mendelian segregation patterns. In contrast, in heterozygous i+/r females, a varying proportion of r chromosomes may irreversibly acquire I factor, independently of classical genetic recombination, by a process called chromosomal contamination. The contaminated reactive chromosomes behave as i  + chromosomes.—In the present paper, evidence is given that the Luminy inducer strain displays a polymorphism for two kinds of second chromosomes. Some of them are i  +, while others, denoted io, are unable t3 induce any SF sterility when introduced by paternal gametes into reactive oocytes. They are also unable to induce contamination of r chromosomes, but, like r chromosomes, they may be contaminated by i+ chromosomes in SF or RSF females. The study of the segregation of i  + and io second chromosomes in the progeny of heterozygous Luminy males and females leads to the conclusion that on chromosome 2 of the Luminy stock the I factor is at a single locus. —XI second and third io chromosomes have been found in several inducer strains. Since these chromosomes can be maintained with i  + chromosomes in inducer strains in spite of their ability to be contaminated in RSF females, it can be concluded that chromosomal contamination does not take place in females of inducer strains. This implies that contamination occurs only in cells having cytoplasm in a reactive state.


Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1867-1878 ◽  
Author(s):  
Emmanuel Gauthier ◽  
Christophe Tatout ◽  
Hubert Pinon

Abstract The I factor (IF) is a LINE-like transposable element from Drosophila melanogaster. IF is silenced in most strains, but under special circumstances its transposition can be induced and correlates with the appearance of a syndrome of female sterility called hybrid dysgenesis. To elucidate the relationship between IF expression and female sterility, different transgenic antisense and/or sense RNAs homologous to the IF ORF1 have been expressed. Increasing the transgene copy number decreases both the expression of an IF-lacZ fusion and the intensity of the female sterile phenotype, demonstrating that IF expression is correlated with sterility. Some transgenes, however, exert their repressive abilities not only through a copy number-dependent zygotic effect, but also through additional maternal and paternal effects that may be induced at the DNA and/or RNA level. Properties of the maternal effect have been detailed: (1) it represses hybrid dysgenesis more efficiently than does the paternal effect; (2) its efficacy increases with both the transgene copy number and the aging of sterile females; (3) it accumulates slowly over generations after the transgene has been established; and (4) it is maintained for at least two generations after transgene removal. Conversely, the paternal effect increases only with female aging. The last two properties of the maternal effect and the genuine existence of a paternal effect argue for the occurrence, in the IF regulation pathway, of a cellular memory transmitted through mitosis, as well as through male and female meiosis, and akin to epigenetic phenomena.


Genetics ◽  
2010 ◽  
Vol 186 (2) ◽  
pp. 669-676 ◽  
Author(s):  
Kyoichi Sawamura ◽  
Kazunori Maehara ◽  
Shotaro Mashino ◽  
Tatsuo Kagesawa ◽  
Miyuki Kajiwara ◽  
...  

1996 ◽  
Vol 16 (5) ◽  
pp. 1966-1977 ◽  
Author(s):  
T Dick ◽  
K Ray ◽  
H K Salz ◽  
W Chia

We report the molecular and genetic characterization of the cytoplasmic dynein light-chain gene, ddlc1, from Drosophila melanogaster. ddlc1 encodes the first cytoplasmic dynein light chain identified, and its genetic analysis represents the first in vivo characterization of cytoplasmic dynein function in higher eucaryotes. The ddlc1 gene maps to 4E1-2 and encodes an 89-amino-acid polypeptide with a high similarity to the axonemal 8-kDa outer-arm dynein light chain from Chlamydomonas flagella. Developmental Northern (RNA) blot analysis and ovary and embryo RNA in situ hybridizations indicate that the ddlc1 gene is expressed ubiquitously. Anti-DDLC1 antibody analyses show that the DDLC1 protein is localized in the cytoplasm. P-element-induced partial-loss-of-function mutations cause pleiotropic morphogenetic defects in bristle and wing development, as well as in oogenesis, and hence result in female sterility. The morphological abnormalities found in the ovaries are always associated with a loss of cellular shape and structure, as visualized by a disorganization of the actin cytoskeleton. Total-loss-of-function mutations cause lethality. A large proportion of mutant animals degenerate during embryogenesis, and the dying cells show morphological changes characteristic of apoptosis, namely, cell and nuclear condensation and fragmentation, as well as DNA degradation. Cloning of the human homolog of the ddlc1 gene, hdlc1, demonstrates that the dynein light-chain 1 is highly conserved in flies and humans. Northern blot analysis and epitope tagging show that the hdlc1 gene is ubiquitously expressed and that the human dynein light chain 1 is localized in the cytoplasm. hdlc1 maps to 14q24.


Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 217-226 ◽  
Author(s):  
Daniel A Barbash ◽  
Michael Ashburner

Abstract Hybrid daughters of crosses between Drosophila melanogaster females and males from the D. simulans species clade are fully viable at low temperature but have agametic ovaries and are thus sterile. We report here that mutations in the D. melanogaster gene Hybrid male rescue (Hmr), along with unidentified polymorphic factors, rescue this agametic phenotype in both D. melanogaster/D. simulans and D. melanogaster/D. mauritiana F1 female hybrids. These hybrids produced small numbers of progeny in backcrosses, their low fecundity being caused by incomplete rescue of oogenesis as well as by zygotic lethality. F1 hybrid males from these crosses remained fully sterile. Hmr+ is the first Drosophila gene shown to cause hybrid female sterility. These results also suggest that, while there is some common genetic basis to hybrid lethality and female sterility in D. melanogaster, hybrid females are more sensitive to fertility defects than to lethality.


Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 157-170 ◽  
Author(s):  
D Adam Mason ◽  
Robert J Fleming ◽  
David S Goldfarb

Abstract Importin α’s mediate the nuclear transport of many classical nuclear localization signal (cNLS)-containing proteins. Multicellular animals contain multiple importin α genes, most of which fall into three conventional phylogenetic clades, here designated α1, α2, and α3. Using degenerate PCR we cloned Drosophila melanogaster importin α1, α2, and α3 genes, demonstrating that the complete conventional importin α gene family arose prior to the split between invertebrates and vertebrates. We have begun to analyze the genetic interactions among conventional importin α genes by studying their capacity to rescue the male and female sterility of importin α2 null flies. The sterility of α2 null males was rescued to similar extents by importin α1, α2, and α3 transgenes, suggesting that all three conventional importin α’s are capable of performing the important role of importin α2 during spermatogenesis. In contrast, sterility of α2 null females was rescued only by importin α2 transgenes, suggesting that it plays a paralog-specific role in oogenesis. Female infertility was also rescued by a mutant importin α2 transgene lacking a site that is normally phosphorylated in ovaries. These rescue experiments suggest that male and female gametogenesis have distinct requirements for importin α2.


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