Spiroplasma effects on Tsetse Flies
Spiroplasma effects on Tsetse Flies
批准号:
10435557
负责人:
Serap AKSOY
金额:
$18.62万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2021
资助国家:
美国
项目状态:
未结题
起止时间:
2021-06-24 至 2025-05-31
关键词:
AddressAffectAfricanAgricultureAnimalsArthropod VectorsArthropodsBacteriaBloodCandidate Disease GeneCollaborationsDataDevelopmentDipteraDiseaseDisease VectorsDynein ATPaseEmbryoEncapsulatedFemaleFertilityFoundationsFrequenciesGene ExpressionGene Expression ProfilingGenesGlandGlossinidaeGonadal structureImmuneImmune responseIndividualInfectionInsectaKnowledgeLaboratoriesLarvaLipidsMedicalMicrobeMidgutMilkMolecularMothersNutrientNutritionalNutritional statusOocytesOvulationParasitesPartner in relationshipPathogenicityPhysiologyPopulationProcessProteinsProteomicsRefractoryReportingReproductionReproductive PhysiologyResearchResistanceSeminal fluidSpermatogoniaSpiroplasmaSubgroupSymbiosisTestingTestisTranslatingTrypanosomaTsetse FliesUgandaUniversitiesUterusWigglesworthiaWolbachiabasecomparativedesigndisease transmissionendosymbiontfitnessflyhuman diseaseinterestmalemale fertilitymating behaviornoveloffspringreproductivereproductive fitnesssocioeconomicssperm cellsuccesstranscriptometranscriptome sequencingtransmission processvectorvector competencevector control
中文摘要
采采蝇是致病性非洲锥虫的主要媒介,其引起社会性疾病。
经济上毁灭性的疾病。采采蝇通过腺营养胎生繁殖,
由共生的内共生体Wigglesperia产生的营养物质。除了Wigglesperia,
一些采采蝇物种可以携带寄生的沃尔巴克氏体和兼性索氏体和螺原体。我们
对沃尔巴克氏体的研究表明,感染这种细菌会影响男性的生殖生理
并诱导细胞质不相容性。在这里,我们解决采采蝇之间的分子对话
和它的新发现的内共生体螺原体,在其他节肢动物中引起各种
生殖异常螺原体只感染须蝇亚属内的采采蝇物种,
包括一种多产病媒Glossina fuscipes fuscipes(Gff)。尽管它对采采蝇的影响
生殖是未知的,螺原体诱导增强的抵抗锥虫感染,
实验室我们提出了两个研究目标,旨在剖析螺旋体感染的影响
1)与交配成功有关的雄性生殖生理学,2)雌性生殖力,3)采采蝇-
螺原体对话,因为它涉及采采蝇的媒介能力。
目标1。螺原体对雄性生殖适合度的影响。我们假设螺原体
雄性舌蝇感染影响1)MAG和睾丸基因表达,2)精包
组成,和3)精子健身。为了验证我们的假设,我们将1)建立螺原体感染
和未感染的Gff系,2)对来自Spi-
3)测定与Spi-或Spi+交配的雌性的精荚含量
雄性,和4)评估螺原体对精子适合度的影响。
目标二。螺原体对寄生虫传播动力学的影响。我们假设
螺原体感染1)通过a)诱导宿主免疫间接削弱了舌蝇的媒介能力
反应或B)限制寄生虫的营养可用性,或2)直接通过表达抗-
锥虫产物。为了验证我们的假设,我们将:1)分析来自GffSpi的全局基因表达-
和GffSpi+个体,2)确定锥虫感染和未感染的GffSpi的营养状况。
和GffSpi+个体和3)测试培养的螺原体的锥虫溶解活性。
增强对采采蝇-螺原体共生的了解将为以下方面提供基础:
阐明不同的生殖内共生体影响宿主生理的机制。
我们的研究结果将有翻译的影响,无论是减少采采蝇繁殖力或载体
能力将直接减少疾病传播。最后,我们的结果将是相关的,
适用于其他在医学和农业上重要的昆虫,其中共生微生物持续存在。
英文摘要
Tsetse flies are prominent vectors of pathogenic African trypanosomes, which cause socio-
economically devastating diseases. Tsetse reproduce by adenotrophic viviparity and depend upon
nutrients produced by their mutualist endosymbiont, Wigglesworthia. In addition to Wigglesworthia,
some tsetse species can harbor parasitic Wolbachia and facultative Sodalis and Spiroplasma. Our
studies on Wolbachia indicate that infection with the bacterium affects male reproductive physiology
and induces Cytoplasmic Incompatibility. Here, we address the molecular dialogue between tsetse
and its newly discovered endosymbiont Spiroplasma, which in other arthropods causes various
reproductive abnormalities. Spiroplasma infects only tsetse species within the Palpalis subgenus,
including Glossina fuscipes fuscipes (Gff), a prolific disease vector. Although its effects on tsetse
reproduction are unknown, Spiroplasma induces enhanced resistance to trypanosome infection in the
laboratory. We propose two research aims designed to dissect the impact of Spiroplasma infections
on 1) male reproductive physiology related to mating success, 2) female fecundity, and 3) tsetse-
Spiroplasma dialogue as it pertains to tsetse’s vector competence.
Aim 1. Spiroplasma effects on male reproductive fitness. We hypothesize that Spiroplasma
infections in male tsetse influence 1) MAG and testis gene expression, 2) spermatophore
composition, and 3) sperm fitness. To test our hypothesis, we will 1) establish Spiroplasma infected
and uninfected Gff lines, 2) perform comparative global gene expression analyses of gonads from Spi-
versus Spi+ males, 3) determine spermatophore contents from the females mated with Spi- or Spi+
males, and 4) evaluate Spiroplasma effects on sperm fitness.
Aim 2. Spiroplasma effects on parasite transmission dynamics. We hypothesize that
Spiroplasma infections diminish tsetse’s vector competence 1) indirectly by a) inducing host immune
responses or b) limiting nutrient availability for parasites, or 2) directly by expressing anti-
trypanosomal products. To test our hypothesis, we will: 1) profile global gene expression from GffSpi-
and GffSpi+ individuals, 2) determine nutritional status of trypanosome infected and uninfected GffSpi-
and GffSpi+ individuals and 3) test cultivated Spiroplasma for trypanolytic activity.
Enhanced knowledge about the tsetse-Spiroplasma symbiosis will provide a foundation to
elucidate the mechanisms by which different reproductive endosymbionts influence host physiology.
Our results will have translational implications, as reducing either tsetse fecundity or vector
competence will directly reduce disease transmission. Finally, our results will be relevant and
applicable to other medically and agriculturally important insects in which symbiotic microbes persist.
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会议论文
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