Sperm plasma membrane breakdown during <i>Drosophila</i> fertilization requires Sneaky, an acrosomal membrane protein

Wilson, Kathleen; Fitch, Karen R.; Bafus, Blaine T.; Wakimoto, Barbara T.

doi:10.1242/dev.02671

Cited by 77 publications

(76 citation statements)

References 44 publications

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“…It is also possible to impose a load if one targets male fertility. In Drosophila there are two genes (misfire and sneaky) that, when disrupted, have the effect of impairing embryo development after fertilization (Ohsako et al 2003;Wilson et al 2006;Smith and Wakimoto 2007). Misfire is needed for correct sperm head decondensation and sneaky is required for the proper breakdown of the sperm plasma membrane.…”

Section: Discussionmentioning

confidence: 99%

The Population Genetics of Using Homing Endonuclease Genes in Vector and Pest Management

2008

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Homing endonuclease genes (HEGs) encode proteins that in the heterozygous state cause doublestrand breaks in the homologous chromosome at the precise position opposite the HEG. If the doublestrand break is repaired using the homologous chromosome, the HEG becomes homozygous, and this represents a powerful genetic drive mechanism that might be used as a tool in managing vector or pest populations. HEGs may be used to decrease population fitness to drive down population densities (possibly causing local extinction) or, in disease vectors, to knock out a gene required for pathogen transmission. The relative advantages of HEGs that target viability or fecundity, that are active in one sex or both, and whose target is expressed before or after homing are explored. The conditions under which escape mutants arise are also analyzed. A different strategy is to place HEGs on the Y chromosome that cause one or more breaks on the X chromosome and so disrupt sex ratio. This strategy can cause severe sex-ratio biases with efficiencies that depend on the details of sperm competition and zygote mortality. This strategy is probably less susceptible to escape mutants, especially when multiple X shredders are used.

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Section: Discussionmentioning

confidence: 99%

The Population Genetics of Using Homing Endonuclease Genes in Vector and Pest Management

2008

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“…We used protein localization methods of Wilson et al (2006). For localization during spermatogenesis, a minimum of three males and five cysts from each male were examined to assess fluorescent signal intensity and variation.…”

Section: Protein Localization During Spermatogenesismentioning

confidence: 99%

The Deadbeat Paternal Effect of Uncapped Sperm Telomeres on Cell Cycle Progression and Chromosome Behavior in Drosophila melanogaster

2016

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Telomere-capping complexes (TCCs) protect the ends of linear chromosomes from illegitimate repair and end-to-end fusions and are required for genome stability. The identity and assembly of TCC components have been extensively studied, but whether TCCs require active maintenance in nondividing cells remains an open question. Here we show that Drosophila melanogaster requires Deadbeat (Ddbt), a sperm nuclear basic protein (SNBP) that is recruited to the telomere by the TCC and is required for TCC maintenance during genome-wide chromatin remodeling, which transforms spermatids to mature sperm. Ddbt-deficient males produce sperm lacking TCCs. Their offspring delay the initiation of anaphase as early as cycle 1 but progress through the first two cycles. Persistence of uncapped paternal chromosomes induces arrest at or around cycle 3. This early arrest can be rescued by selective elimination of paternal chromosomes and production of gynogenetic haploid or haploid mosaics. Progression past cycle 3 can also occur if embryos have reduced levels of the maternally provided checkpoint kinase Chk2. The findings provide insights into how telomere integrity affects the regulation of the earliest embryonic cell cycles. They also suggest that other SNBPs, including those in humans, may have analogous roles and manifest as paternal effects on embryo quality.KEYWORDS telomere maintenance; telomere capping; cell cycle checkpoint; paternal effect; sperm nuclear basic protein T ELOMERES are the natural ends of linear chromosomes and have distinct properties from broken ends. Multiple proteins are enriched predominantly, if not exclusively, at telomeres and form a capping complex that protects telomeric DNA from engaging in aberrant DNA repair activities. Protein components of the telomere-capping complex (TCC) vary among organisms, in part because species differ in telomeric sequences and whether telomeres are maintained by telomerase or alternative mechanisms (Raffa et al. 2011;Mason et al. 2015). Nonetheless, the TCC's essential functions are well conserved. Failure to assemble TCCs results in telomeric DNA degradation, telomere fusions, and genomic instability.Mutations in at least 12 loci of Drosophila melanogaster lead to telomere fusions in neuroblasts. Their analysis has led to the identification of telomere-enriched and telomereexclusive proteins required for telomere elongation or TCC assembly, maintenance, or function (Cenci et al. 2005;Pimpinelli 2006). Absence of any one component results in telomere fusions but components have distinct activities (Pimpinelli 2006). For example, heterochromatin protein 1a (HP1a) binds modified histone H3-MeK9 and represses transcription of telomeric retrotransposons and telomere elongation. HP1a also binds DNA and this activity is required for its capping function. The TCC protein HOAP binds DNA and HP1a. Although HOAP is required for capping, it does not affect retrotransposon transcription or telomere elongation. A third protein, HipHop, binds both HP1a and HOAP. HOAP and HipHo...

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“…The mammalian DC-STAMP protein is required for osteoclast precursor cell fusion (Kukita et al, 2004). It is striking that another DC-STAMP domain protein Sneaky is an acrosomal membrane protein that is required for plasma membrane breakdown during Drosophila fertilization (Wilson et al, 2006). It is an intriguing possibility that SPE-42 is in some way mediating C. elegans sperm-egg fusion.…”

Section: Spe-42 Encodes a Dc-stamp Domain Seven-pass Integral Membranmentioning

confidence: 99%

Genes required for the common miracle of fertilization in Caenorhabditis elegans

Singson¹,

Hang²,

Parry³

2008

Int. J. Dev. Biol.

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Fertilization involves multiple layers of sperm-egg interactions that lead to gamete fusion and egg activation. There must be specific molecules required for these interactions. The challenge is to determine the identity of the genes encoding these molecules and how their protein products function. The nematode worm Caenorhabditis elegans has emerged as an efficient model system for gene discovery and understanding the molecular mechanisms of fertilization. The primary advantage of the C. elegans system is the ability to isolate and maintain mutants that affect sperm or eggs and no other cells. In this review we describe progress and challenges in the analysis of genes required for gamete interactions and egg activation in the worm.

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Sperm plasma membrane breakdown during Drosophila fertilization requires Sneaky, an acrosomal membrane protein

Cited by 77 publications

References 44 publications

The Population Genetics of Using Homing Endonuclease Genes in Vector and Pest Management

The Population Genetics of Using Homing Endonuclease Genes in Vector and Pest Management

The Deadbeat Paternal Effect of Uncapped Sperm Telomeres on Cell Cycle Progression and Chromosome Behavior in Drosophila melanogaster

Genes required for the common miracle of fertilization in Caenorhabditis elegans

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