Relevant bibliographies by topics / Drosophila Drosophila Drosophila Infertility, Male

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters

Academic literature on the topic 'Drosophila Drosophila Drosophila Infertility, Male'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Drosophila Drosophila Drosophila Infertility, Male"

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Wu, Hao, Liwei Sun, Yang Wen, Yujuan Liu, Jun Yu, Feiyu Mao, Ya Wang, et al. "Major spliceosome defects cause male infertility and are associated with nonobstructive azoospermia in humans." Proceedings of the National Academy of Sciences 113, no. 15 (March 28, 2016): 4134–39. http://dx.doi.org/10.1073/pnas.1513682113.

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Processing of pre-mRNA into mRNA is an important regulatory mechanism in eukaryotes that is mediated by the spliceosome, a huge and dynamic ribonucleoprotein complex. Splicing defects are implicated in a spectrum of human disease, but the underlying mechanistic links remain largely unresolved. Using a genome-wide association approach, we have recently identified single nucleotide polymorphisms in humans that associate with nonobstructive azoospermia (NOA), a common cause of male infertility. Here, using genetic manipulation of corresponding candidate loci in Drosophila, we show that the spliceosome component SNRPA1/U2A is essential for male fertility. Loss of U2A in germ cells of the Drosophila testis does not affect germline stem cells, but does result in the accumulation of mitotic spermatogonia that fail to differentiate into spermatocytes and mature sperm. Lack of U2A causes insufficient splicing of mRNAs required for the transition of germ cells from proliferation to differentiation. We show that germ cell-specific disruption of other components of the major spliceosome manifests with the same phenotype, demonstrating that mRNA processing is required for the differentiation of spermatogonia. This requirement is conserved, and expression of human SNRPA1 fully restores spermatogenesis in U2A mutant flies. We further report that several missense mutations in human SNRPA1 that inhibit the assembly of the major spliceosome dominantly disrupt spermatogonial differentiation in Drosophila. Collectively, our findings uncover a conserved and specific requirement for the major spliceosome during the transition from spermatogonial proliferation to differentiation in the male testis, suggesting that spliceosome defects affecting the differentiation of human spermatogonia contribute to NOA.
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Morton, David B., Rachel Clemens-Grisham, Dennis J. Hazelett, and Anke Vermehren-Schmaedick. "Infertility and Male Mating Behavior Deficits Associated With Pde1c in Drosophila melanogaster." Genetics 186, no. 1 (June 15, 2010): 159–65. http://dx.doi.org/10.1534/genetics.110.118018.

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Siddall, N. A., and G. R. Hime. "A Drosophila toolkit for defining gene function in spermatogenesis." Reproduction 153, no. 4 (April 2017): R121—R132. http://dx.doi.org/10.1530/rep-16-0347.

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Expression profiling and genomic sequencing methods enable the accumulation of vast quantities of data that relate to the expression of genes during the maturation of male germ cells from primordial germ cells to spermatozoa and potential mutations that underlie male infertility. However, the determination of gene function in specific aspects of spermatogenesis or linking abnormal gene function with infertility remain rate limiting, as even in an era of CRISPR analysis of gene function in mammalian models, this still requires considerable resources and time. Comparative developmental biology studies have shown the remarkable conservation of spermatogenic developmental processes from insects to vertebrates and provide an avenue of rapid assessment of gene function to inform the potential roles of specific genes in rodent and human spermatogenesis. The vinegar fly, Drosophila melanogaster, has been used as a model organism for developmental genetic studies for over one hundred years, and research with this organism produced seminal findings such as the association of genes with chromosomes, the chromosomal basis for sexual identity, the mutagenic properties of X-irradiation and the isolation of the first tumour suppressor mutations. Drosophila researchers have developed an impressive array of sophisticated genetic techniques for analysis of gene function and genetic interactions. This review focuses on how these techniques can be utilised to study spermatogenesis in an organism with a generation time of 9 days and the capacity to introduce multiple mutant alleles into an individual organism in a relatively short time frame.
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Tao, Yun, Zhao-Bang Zeng, Jian Li, Daniel L. Hartl, and Cathy C. Laurie. "Genetic Dissection of Hybrid Incompatibilities BetweenDrosophila simulansandD. mauritiana. II. Mapping Hybrid Male Sterility Loci on the Third Chromosome." Genetics 164, no. 4 (August 1, 2003): 1399–418. http://dx.doi.org/10.1093/genetics/164.4.1399.

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AbstractHybrid male sterility (HMS) is a rapidly evolving mechanism of reproductive isolation in Drosophila. Here we report a genetic analysis of HMS in third-chromosome segments of Drosophila mauritiana that were introgressed into a D. simulans background. Qualitative genetic mapping was used to localize 10 loci on 3R and a quantitative trait locus (QTL) procedure (multiple-interval mapping) was used to identify 19 loci on the entire chromosome. These genetic incompatibilities often show dominance and complex patterns of epistasis. Most of the HMS loci have relatively small effects and generally at least two or three of them are required to produce complete sterility. Only one small region of the third chromosome of D. mauritiana by itself causes a high level of infertility when introgressed into D. simulans. By comparison with previous studies of the X chromsome, we infer that HMS loci are only ∼40% as dense on this autosome as they are on the X chromosome. These results are consistent with the gradual evolution of hybrid incompatibilities as a by-product of genetic divergence in allopatric populations.
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Chow, Clement Y., Frank W. Avila, Andrew G. Clark, and Mariana F. Wolfner. "Induction of Excessive Endoplasmic Reticulum Stress in the Drosophila Male Accessory Gland Results in Infertility." PLOS ONE 10, no. 3 (March 5, 2015): e0119386. http://dx.doi.org/10.1371/journal.pone.0119386.

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Camper, Sally A., Michelle L. Brinkmeier, Krista A. Geister, Morgan Jones, and Ivan Maillard. "Mice Deficient in a Drosophila Homeotic Selector Ortholog Exhibit Female Infertility and Reduced Male Fertility." Biology of Reproduction 83, Suppl_1 (November 1, 2010): 313. http://dx.doi.org/10.1093/biolreprod/83.s1.313.

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Lin, T. Y., S. Viswanathan, C. Wood, P. G. Wilson, N. Wolf, and M. T. Fuller. "Coordinate developmental control of the meiotic cell cycle and spermatid differentiation in Drosophila males." Development 122, no. 4 (April 1, 1996): 1331–41. http://dx.doi.org/10.1242/dev.122.4.1331.

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Wild-type function of four Drosophila genes, spermatocyte arrest, cannonball, always early and meiosis I arrest, is required both for cell-cycle progression through the G2/M transition of meiosis I in males and for onset of spermatid differentiation. In males mutant for any one of these meiotic arrest genes, mature primary spermatocytes with partially condensed chromosomes accumulate and postmeiotic cells are lacking. The arrest in cell-cycle progression occurs prior to degradation of cyclin A protein. The block in spermatogenesis in these mutants is not simply a secondary consequence of meiotic cell-cycle arrest, as spermatid differentiation proceeds in males mutant for the cell cycle activating phosphatase twine. Instead, the arrest of both meiosis and spermiogenesis suggests a control point that may serve to coordinate the male meiotic cell cycle with the spermatid differentiation program. The phenotype of the Drosophila meiotic arrest mutants is strikingly similar to the histopathological features of meiosis I maturation arrest infertility in human males, suggesting that the control point may be conserved from flies to man.
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Zouros, E. "Advances in the genetics of reproductive isolation in Drosophila." Genome 31, no. 1 (January 1, 1989): 211–20. http://dx.doi.org/10.1139/g89-036.

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Speciation genetics is defined as the study of genetic events and processes that differentiate the probabilities that genetic material from individual members of a population will co-occur in individuals of some future generation. It follows that phenotypic attributes that contribute to this differentiation of probabilities (e.g., mating preferences, sterility, or infertility of individuals from certain types of matings) constitute the phenotype of speciation, and genetic loci that may affect these phenotypic attributes can be considered as speciation genes. The literature on genetic differences between hybridizable species of Drosophila that are responsible for morphological differences, mating preferences, hybrid inviability, and hybrid sterility are reviewed with special reference to the species pair D. mojavensis – D. arizonensis. The case for the involvement of karyotypic changes in speciation in rodents is briefly discussed. It is concluded that no major advance has been made in the speciation genetics of Drosophila since Dobzhansky initiated the field 40 years ago. Yet, the identification of several gene loci that cause hybrid inviability or sterility may open the way to the understanding of reproductive isolation at the molecular level. It is not clear whether this approach will lead to general molecular mechanisms underlying the speciation process.Key words: speciation genetics, hybrid sterility, reproductive isolation, Drosophila.
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NOOR, MOHAMED A. F. "Patterns of evolution of genes disrupted in expression in Drosophila species hybrids." Genetical Research 85, no. 2 (April 2005): 119–25. http://dx.doi.org/10.1017/s0016672305007500.

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Divergence between species in regulatory pathways may contribute to hybrid incompatibilities such as sterility. Consistent with this idea, genes involved in male fertility often evolve faster than most other genes both in amino acid sequence and in expression. Previously, we identified a panel of male-specific genes underexpressed in sterile male hybrids of Drosophila simulans and D. mauritiana relative to pure species, and we showed that this underexpression is associated with infertility. In a preliminary effort to assess the generalities in the patterns of evolution of these genes, I examined patterns of mRNA expression in three of these genes in sterile F1 hybrid males of D. pseudoobscura and D. persimilis. F1 hybrid males bearing D. persimilis X chromosomes underexpressed all these genes relative to the parental species, while hybrids bearing D. pseudoobscura X chromosomes underexpressed two of these three genes. Interestingly, the third gene, CG5762, has undergone extensive amino acid evolution within the D. pseudoobscura species group, possibly driven by positive natural selection. We conclude that some of the same genes exhibit disruptions in expression within each of the two species groups, which could suggest commonalities in the regulatory architecture of sterility in these groups. Alternative explanations are also considered.
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Mason, D. Adam, Robert J. Fleming, and David S. Goldfarb. "Drosophila melanogaster Importin α1 and α3 Can Replace Importin α2 During Spermatogenesis but Not Oogenesis." Genetics 161, no. 1 (May 1, 2002): 157–70. http://dx.doi.org/10.1093/genetics/161.1.157.

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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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Dissertations / Theses on the topic "Drosophila Drosophila Drosophila Infertility, Male"

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Harbison, Diane T. "Male-specific transcripts from Drosophila melanogaster." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337508.

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Bentley, Joanna Kate. "The interaction between male-killing spiroplasma and 'Drosophila'." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409219.

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Walker, Michael John. "Proteins of the male accessory gland of Drosophila melanogaster." Thesis, University of Leeds, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485188.

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In Drosophila melanogaster, the male seminal fluid contains proteins that are important for reproductive success. Many of these proteins are synthesised by the male accessory glands and are secreted into the accessory gland lumen, where they are stored until required. Previous studies on the identification of Drosophila accessory gland' proteins have largely focused on characterisation of male-specific accessory gland cDNAs from D. melanogaster and, moni···.recently, Drosophila simulans. The work presented in this' thesis identified thirty proteins in the accessory gland of D. melanogaster. Fourteen proteins have predicted secretory signals and thus are secreted accessory gland proteins. They included protein-folding and stressresponse proteins, a hormone, a lipase, a serpin, a cysteine-rich protein and three peptidases, a pro-enzyme form of a cathepsin K-like cysteine peptidase, Angiotensin converting enzyme and a y-glutamyl transpeptidase. Biochemical assays of the peptidase levels show the y-glutamyl transpeptidase and Angiotensin converting enzyme are reduced in mated males accessory gland suggesting their prescence in the seminal fluid. The ultrastructure of the accessory gland and secretions were investigated by electron microscopy. The filamentous contents of the secondary cells and lumen were studied by negative staining electron microscopy and cryo-electron microscopy as well as by proteomic methodologies. The major protein component of the filaments was identified as Acp36DE, which is known to be involved in sperm storage thus suggesting that is the role for the filaments.
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Reed, Laura Katie. "The Genetic Relationships of the Sister Species Drosophila Mojavensis and Drosophila Arizonae and the Genetic Basis of Sterility in their Hybrid Males." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/194437.

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The cactophilic Drosophila mojavensis species group living in the deserts and dry tropical forests of the Southwestern United States and Mexico provides a valuable system for studies in diversification and speciation. My dissertation addresses a variety of evolutionary genetic questions using this system.Rigorous studies of the relationships between host races of D. mojavensis and the relationships among the members of the species group (D. mojavensis, D. arizona, and D. navojoa) are lacking. I used mitochondrial CO1 sequence data to address the phylogenetics and population genetics of this species group (Appendix A). In this study I have found that the sister species D. mojavensis and D. arizonae share no mitochondrial haplotypes and thus show no evidence for recent introgression. I estimate the divergence time between D. mojavensis and D. arizonae to be between 0.66 and 0.99 million years ago. I performed additional population genetic analyses of these species to provide a basis for future hypothesis testing.In Appendix B, I report the first example of substantial intraspecific polymorphism for genetic factors contributing to hybrid male sterility. I show that the occurrence of hybrid male sterility in crosses between Drosophila mojavensis and its sister species, D. arizonae is controlled by factors present at different frequencies in different populations of D. mojavensis. In addition, I show that hybrid male sterility is a complex phenotype; some hybrid males with motile sperm still cannot sire offspring.The large degree of variation between isofemale lines in producing sterile hybrid sons suggests a complex genetic basis to hybrid male sterility warranting quantitative genetic analysis. Since the genes underlying hybrid male sterility in these species are not yet fixed, I am able to perform explicit genetic analysis of this reproductive isolating mechanism. In Appendix C, I present the results of mapping QTL for hybrid male sterility within species. The genetic architecture underlying hybrid male sterility when analyzed directly in the F1 is highly complex. Thus, hybrid male sterility arises as a complex trait in this system and we propose a drift-based model for the evolution of this phenotype.
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El, Sharnouby Sherif Maher. "Methodology for genome-wide epigenetic profiling of the Drosophila male germline." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609941.

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Innocenti, Paolo. "Sexual Conflict and Gene Expression in Drosophila melanogaster." Doctoral thesis, Uppsala universitet, Zooekologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-156567.

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Sexual conflict is broadly defined as a conflict between the evolutionary interests of the two sexes. Depending on the genetic architecture of the traits involved, it can occur at the level of male-female interactions or take the form of selection acting to change the mean of a shared trait against the sign of its genetic correlation. The aim of my thesis was to use genome-wide expression profiles in the model organism Drosophila melanogaster to provide novel insights in the study of sexual conflict. First, we studied the female post-mating response to partition transcriptional changes associated with reproduction from male-induced effects, which are known to be harmful to females. We found substantial changes in expression of metabolic pathways associated with the activation of reproduction, while male-specific effects were dominated by the onset of an immune response. Changes in female response under different mating strategies was studied using experimental evolution: we found that monogamous females suffered decreased fecundity and their gene expression profiles suggested an overall weaker response to mating. To identify sexually antagonistic genes, we used hemiclonal lines and associated their sex-specific fitness with genome-wide transcript abundance. We confirmed the presence of a negative covariance for fitness and identified a group of candidate genes experiencing sexually antagonistic selection. We then focused on mitochondria, which can enable the accumulation of deleterious mutations with sex-specific effects due to their maternal inheritance, and found few effects on nuclear gene expression in females but major effects in males, predominantly in male-specific tissues. Finally, we used published data to compare intraspecific and interspecific genetic variation for a set of transcripts, to test whether speciation occurs along lines of maximum genetic variance. In conclusion, gene expression techniques can generate useful results in the study of sexual conflict, particularly in association with phenotypic data or when integrated with published datasets.
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Pavlou, Hania Jamil. "Intersecting doublesex neurons underlying sexual behaviours in Drosophila melanogaster." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5e193063-fcea-4652-b8ad-25632b379298.

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In Drosophila, the functionally conserved transcription factor, doublesex (dsx), is pivotal to the specification of sexual identity in both males and females. One of its key dedicated roles involves regulating the development of a sexually dimorphic nervous system (NS) that underlies both male and female reproductive behaviours. Specific inhibition of the function of dsx-expressing neurons in males and females results in a global disruption of these sex-specific behavioural outputs. However, little is known about the functional organisation of this dsx circuit that encodes the potential to display these behaviours. Such investigations require the generation of a novel transgenic tool, capable of separating the function of dsx in the NS from that of the body. To achieve this, I generated a novel split-GAL4 dsxGAL4-DBD hemidriver by ends in homologous recombination. Coupling the novel tool with the pan-neuronal elavVP16-AD hemidriver, revealed spatial restriction of dsxGAL4-DBD/elavVP16-AD expression to dsx neurons only; enabling the realisation of novel patterns of dsx-expression in the peripheral NS. Next, the ability to elicit male-specific behavioural outputs upon activation of all dsx neurons formed the basis of a large behavioural screen aimed at parsing dsx circuitry into functionally distinct clusters. I utilised the novel dsxGAL4-DBD hemidriver to screen a large collection of extant enhancer trap lines (ETVP16-AD), for the elicitation of distinct sub-behaviours of male courtship. Here, I show that the activity of dsx-expressing clusters in: i) the brain (dsx-pC1, -pC2 and -pC3 collectively) regulate the early steps of male courtship (initiation, orientation and wing extension), ii) the pro- and mesothoracic ganglia (dsx-TN1 and -TN2) regulate the middle steps of male courtship (wing extension and possibly courtship song) and iii) the abdominal ganglia (dsx-Abg) regulate the late steps of male courtship (abdominal curling, attempted copulation and copulation). These data establish functional correlations between dsx clusters in distinct neuroanatomical foci and specific sub-behaviours of the courtship repertoire. Furthermore, the novel intersectional tool primed a collaborative study on female post-copulatory behaviours. We identified key sensory neurons in the female reproductive tract involved in initiating post-mating behaviours. Subsequent functional interrogations of dsx circuitry in the central NS revealed a subset of dsx-expressing neurons in the Abg that mediate changes in the female behavioural repertoire after mating. Characterisation of this relatively simple neural circuitry sheds light on the organisation of the fly brain. Ultimately, future studies will define principles of neural circuit operation, which may be similarly conserved in the nervous systems of higher animals.
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White, Alison. "Assessing Territoriality as a Component of Male Sexual Fitness in 'Drosophila serrata'." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24020.

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While the phenotypic effects of sexual selection have been well studied, the consequences for population mean fitness remain unclear. Additionally, there is a need to more fully characterize how various forms of inter- and intrasexual selection combine to affect the evolution of traits under sexual selection. Here, I address these issues as they relate to male territoriality in Drosophila serrata, a model system for the study of female preference for male pheromones. First, I demonstrate that territoriality occurs and is a likely component of male sexual fitness. Results from a phenotypic manipulation indicate that territorial success was also condition-dependent, and that sexual selection against low condition males tended to be stronger given a high opportunity for territory defense. Territorial success depended on body size but not on pheromones. How this and other components of male mating success interact to affect trait evolution and population mean fitness remains an important area for future study.
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Billeter, Jean-Christophe. "Targeting fruitless neurons : neurogenetic dissection of male sexual behaviour in Drosophila melanogaster." Thesis, University of Glasgow, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411778.

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Rylett, Caroline McGinn. "Peptidases of the testes and accessory glands of the male Drosophila melanogaster." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434584.

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Books on the topic "Drosophila Drosophila Drosophila Infertility, Male"

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Hughes, Kimberly A. Evolutionary genetics of male life history traits in Drosophila melanogaster. 1993.

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Book chapters on the topic "Drosophila Drosophila Drosophila Infertility, Male"

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Bonaccorsi, Silvia, and Maurizio Gatti. "Drosophila Male Meiosis." In Methods in Molecular Biology, 277–88. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6340-9_16.

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Yamamoto, Daisuke, Kazue Usui-Aoki, and Seigo Shima. "Male-specific expression of the Fruitless protein is not common to all Drosophila species." In Drosophila melanogaster, Drosophila simulans: So Similar, So Different, 267–72. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-94-007-0965-2_23.

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Bin, Chen. "Mapping of Drosophila Mutations Using Site-specific Male Recombination." In Grauzone and Completion of Meiosis During Drosophila Oogenesis, 11–29. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1409-1_2.

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Singh, Shree Ram, and Steven X. Hou. "Immunohistological Techniques for Studying the Drosophila Male Germline Stem Cell." In Methods in Molecular Biology™, 45–59. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-214-8_3.

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Toledano, Hila, and D. Leanne Jones. "Age-Related Changes to Drosophila m. Male Germline Stem Cells." In Stem Cell Aging: Mechanisms, Consequences, Rejuvenation, 71–84. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1232-8_4.

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Inaba, Mayu, and Yukiko M. Yamashita. "Evaluation of the Asymmetric Division of Drosophila Male Germline Stem Cells." In Methods in Molecular Biology, 49–62. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-4017-2_3.

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Papagiannouli, Fani, and Ingrid Lohmann. "The Male Stem Cell Niche: Insights from Drosophila and Mammalian Model Systems." In Tissue-Specific Stem Cell Niche, 281–311. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21705-5_12.

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Tompkins, Laurie. "The Development of Male- and Female-Specific Sexual Behavior in Drosophila melanogaster." In Genome Analysis in Eukaryotes, 120–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-11829-0_6.

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Polak, Michael. "Parasites increase fluctuating asymmetry of male Drosophila nigrospiracula: implications for sexual selection." In Developmental Instability: Its Origins and Evolutionary Implications, 257–67. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0830-0_20.

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Liebrich, W., and N. Kociok. "The Possible Role of the Y Chromosome During Male Germ Cell Differentiation in Drosophila." In Invertebrate and Fish Tissue Culture, 104–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73626-1_25.

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