scholarly journals The Effect on Embryogenesis of a Sex-linked Female-Sterility Factor in Drosophila melanogaster

Development ◽  
1957 ◽  
Vol 5 (4) ◽  
pp. 404-421
Author(s):  
S. J. Counce ◽  
D. A. Ede
Keyword(s):  
Drosophila Melanogaster ◽  
Adult Stage ◽  
Female Sterility ◽  
Homozygous Mutant ◽  
Hereditary Factors ◽  
Adult Organism ◽  
Or Genes ◽  
Mutant Male ◽  
Sterility Genes ◽  
Orderly Arrangement

Waddington (1956) has called attention to the importance of the relation between the structure of the egg and hereditary factors which determine characters in the developing organism: ‘When we discuss the eggs of the different kinds of animals, we…find that the eventual origin from which the whole later development springs is the orderly arrangement of essential parts of the ovum. We must therefore enquire a little more deeply how this arrangement is brought about. In particular, what is the relation between it and the hereditary factors or genes which determine the detailed character of the adult organism?’ Although, in most animals, no such relations have been carefully studied (with the exception of direction of coiling in Limnea) there exists in Drosophila a class of female-sterility genes or factors in which females are sterile because the egg cytoplasm will not support the development of a viable zygote (Lynch, 1919; Merrell, 1947; Counce, 1956 a, b, c); e.g. when a female heterozygous for the gene is mated to a mutant male, females homozygous for the factor develop into adults; however, when these homozygous mutant females are mated, their offspring never develop to an adult stage.

scholarly journals Sterile mutation in Drosophila melanogaster

1977 ◽  
Vol 30 (2) ◽  
pp. 107-113 ◽  
Author(s):  
Takao K. Watanabe ◽  
Won Ho Lee
Keyword(s):  
Drosophila Melanogaster ◽  
Male Sterility ◽  
Female Sterility ◽  
Sterility Genes ◽  
Lethal Genes

SUMMARYThe number of loci which are potentially able to produce sterility genes was estimated for Drosophila melanogaster. There appear to be, on the second chromosome, about 80 loci capable of producing male sterility and about 60 loci capable of producing female sterility. These figures seem to be considerably less than (400–500) loci responsible for lethal genes.

scholarly journals Introgression of Drosophila simulans Nuclear Pore Protein 160 in Drosophila melanogaster Alone Does Not Cause Inviability but Does Cause Female Sterility

Genetics ◽  
2010 ◽  
Vol 186 (2) ◽  
pp. 669-676 ◽  
Author(s):  
Kyoichi Sawamura ◽  
Kazunori Maehara ◽  
Shotaro Mashino ◽  
Tatsuo Kagesawa ◽  
Miyuki Kajiwara ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Drosophila Simulans ◽  
Female Sterility ◽  
Nuclear Pore ◽  
Nuclear Pore Protein ◽  
Pore Protein

XXVII.—The Inheritance of Long and Short Wings in the Weevil, Sitona hispidula, with a Discussion of Wing Reduction among Beetles

1928 ◽  
Vol 55 (3) ◽  
pp. 665-735 ◽  
Author(s):  
Dorothy J. Jackson
Keyword(s):  
Experimental Work ◽  
Adult Stage ◽  
Point Of View ◽  
The Other ◽  
Wing Dimorphism ◽  
Wing Reduction ◽  
Hereditary Factors ◽  
The Subject ◽  
The One ◽  
Evolutionary Point

It is well known that in many orders of typically winged insects species occur which in the adult stage are apterous or have the wings so reduced in size that flight is impossible. Sometimes the reduction of wings affects one sex only, as in the case of the females of certain moths, but in the majority of cases it is exhibited by both sexes. In many instances wing dimorphism occurs irrespective of sex, one form of the species having fully developed wings and the other greatly reduced wings. In some species the wings are polymorphic. The problem of the origin of reduced wings and of other functionless organs is one of great interest from the evolutionary point of view. Various theories have been advanced in explanation, but in the majority of cases the various aspects of the subject are too little known to warrant discussion. More experimental work is required to show how far environmental conditions on the one hand, and hereditary factors on the other, are responsible for this phenomenon. Those species which exhibit alary dimorphism afford material for the study of the inheritance of the two types of wings, but only in a few cases has this method of research been utilized.

scholarly journals Cytoplasmic dynein (ddlc1) mutations cause morphogenetic defects and apoptotic cell death in Drosophila melanogaster.

1996 ◽  
Vol 16 (5) ◽  
pp. 1966-1977 ◽  
Author(s):  
T Dick ◽  
K Ray ◽  
H K Salz ◽  
W Chia
Keyword(s):  
Drosophila Melanogaster ◽  
Light Chain ◽  
Blot Analysis ◽  
Cytoplasmic Dynein ◽  
P Element ◽  
Female Sterility ◽  
Dynein Light Chain ◽  
Loss Of Function ◽  
Light Chain Gene

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.

The Post-embryonic Development of the Tracheal System in Drosophila melanogaster

1957 ◽  
Vol s3-98 (41) ◽  
pp. 123-150
Author(s):  
JOAN M. WHITTEN
Keyword(s):  
Drosophila Melanogaster ◽  
Adult Stage ◽  
Larval Instar ◽  
Pupal Stage ◽  
Tracheal System ◽  
True Nature ◽  
The Third ◽  
Air Sacs ◽  
Abdominal Region ◽  
Pupal Cuticle

The fate of the tracheal system is traced from the first larval instar to the adult stage. The basic larval pattern conforms to that shown for other Diptera Cyclorrhapha (Whitten, 1955), and is identical in all three instars. According to previous accounts the adult system directly replaces the larval: the larval system is partly shed, partly histolysed, and the adult system arises from imaginal cell clusters independently of the preceding larval system. In contrast, it is shown here that in the cephalic, thoracic, and anterior abdominal region there is a definite continuity in the tracheal system, from larval, through pupal to the adult stage, whereas in the posterior abdominal region the larval system is histolysed, and the adult system is independent of it in origin. Moreover, in the pupal stage this region is tracheated by tracheae arising from the anterior abdominal region and belonging to a distinct pupal system. Moulting of the tracheal linings is complete at the first and second larval ecdyses, but incomplete at the third larval-pupal and pupal-adult ecdyses. In consequence, in both pupal and adult systems there are tracheae which are secreted around preexisting tracheae, others formed as new ‘branch’ tracheae, and those which have been carried over from the previous instar. In the adult the newly formed tracheae of the posterior abdominal region fall into a fourth category. Most of the adult thoracic air sacs correspond to new ‘branch’ tracheae of other instars. The pre-pupal moult and instar are discussed with reference to the tracheal system and tentative suggestions are made concerning the true nature of the pre-pupal cuticle. There is no pre-pupal tracheal system. Events traced for Drosophila would seem to be general for Cyclorrhapha, both Acalypterae and Calypterae. The separate fates of the anterior and posterior abdom inal systems, in contrast with the straightforward development in Dipterc Nematocera, would appear to mark a distinct step in the evolution of the system in Diptera.

A Novel System of Fertility Rescue in Drosophila Hybrids Reveals a Link Between Hybrid Lethality and Female Sterility

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 217-226 ◽  
Author(s):  
Daniel A Barbash ◽  
Michael Ashburner
Keyword(s):  
Drosophila Melanogaster ◽  
Low Temperature ◽  
Genetic Basis ◽  
Female Sterility ◽  
Hybrid Lethality ◽  
Hybrid Male ◽  
Hybrid Female ◽  
F1 Hybrid ◽  
Drosophila Gene

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.

Drosophila melanogaster Importin α1 and α3 Can Replace Importin α2 During Spermatogenesis but Not Oogenesis

Genetics ◽  
2002 ◽  
Vol 161 (1) ◽  
pp. 157-170 ◽  
Author(s):  
D Adam Mason ◽  
Robert J Fleming ◽  
David S Goldfarb
Keyword(s):  
Drosophila Melanogaster ◽  
Female Sterility ◽  
Degenerate Pcr ◽  
Male And Female ◽  
Importin Α ◽  
Localization Signal ◽  
Male And Female Sterility ◽  
A Site ◽  
Female Gametogenesis

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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