Using a Combination of Novel Research Tools to Understand Social Interaction in the Drosophila melanogaster Model for Fragile X Syndrome

Biology Pub Date : 2024-06-12 DOI:10.3390/biology13060432
Maja Stojković, Milan Petrovic, Maria Capovilla, Sara Milojevic, Vedrana Makevic, D. Budimirovic, Louise Corscadden, Shuhan He, D. Protic
{"title":"Using a Combination of Novel Research Tools to Understand Social Interaction in the Drosophila melanogaster Model for Fragile X Syndrome","authors":"Maja Stojković, Milan Petrovic, Maria Capovilla, Sara Milojevic, Vedrana Makevic, D. Budimirovic, Louise Corscadden, Shuhan He, D. Protic","doi":"10.3390/biology13060432","DOIUrl":null,"url":null,"abstract":"Fragile X syndrome (FXS), the most common monogenic cause of inherited intellectual disability and autism spectrum disorder, is caused by a full mutation (>200 CGG repeats) in the Fragile X Messenger Ribonucleoprotein 1 (FMR1) gene. Individuals with FXS experience various challenges related to social interaction (SI). Animal models, such as the Drosophila melanogaster model for FXS where the only ortholog of human FMR1 (dFMR1) is mutated, have played a crucial role in the understanding of FXS. The aim of this study was to investigate SI in the dFMR1B55 mutants (the groups of flies of both sexes simultaneously) using the novel Drosophila Shallow Chamber and a Python data processing pipeline based on social network analysis (SNA). In comparison with wild-type flies (w1118), SNA analysis in dFMR1B55 mutants revealed hypoactivity, fewer connections in their networks, longer interaction duration, a lower ability to transmit information efficiently, fewer alternative pathways for information transmission, a higher variability in the number of interactions they achieved, and flies tended to stay near the boundaries of the testing chamber. These observed alterations indicate the presence of characteristic strain-dependent social networks in dFMR1B55 flies, commonly referred to as the group phenotype. Finally, combining novel research tools is a valuable method for SI research in fruit flies.","PeriodicalId":504576,"journal":{"name":"Biology","volume":"48 12","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/biology13060432","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Fragile X syndrome (FXS), the most common monogenic cause of inherited intellectual disability and autism spectrum disorder, is caused by a full mutation (>200 CGG repeats) in the Fragile X Messenger Ribonucleoprotein 1 (FMR1) gene. Individuals with FXS experience various challenges related to social interaction (SI). Animal models, such as the Drosophila melanogaster model for FXS where the only ortholog of human FMR1 (dFMR1) is mutated, have played a crucial role in the understanding of FXS. The aim of this study was to investigate SI in the dFMR1B55 mutants (the groups of flies of both sexes simultaneously) using the novel Drosophila Shallow Chamber and a Python data processing pipeline based on social network analysis (SNA). In comparison with wild-type flies (w1118), SNA analysis in dFMR1B55 mutants revealed hypoactivity, fewer connections in their networks, longer interaction duration, a lower ability to transmit information efficiently, fewer alternative pathways for information transmission, a higher variability in the number of interactions they achieved, and flies tended to stay near the boundaries of the testing chamber. These observed alterations indicate the presence of characteristic strain-dependent social networks in dFMR1B55 flies, commonly referred to as the group phenotype. Finally, combining novel research tools is a valuable method for SI research in fruit flies.
综合利用多种新型研究工具了解脆性 X 综合征黑腹果蝇模型中的社会交互作用
脆性 X 综合征(FXS)是导致遗传性智力障碍和自闭症谱系障碍的最常见的单基因病因,由脆性 X 信使核糖核蛋白 1(FMR1)基因的全突变(>200 CGG 重复)引起。FXS 患者在社会交往(SI)方面会遇到各种挑战。动物模型,如黑腹果蝇的 FXS 模型(人类 FMR1(dFMR1)的唯一直向同源物发生了突变)在了解 FXS 方面发挥了至关重要的作用。本研究的目的是利用新型果蝇浅室和基于社会网络分析(SNA)的 Python 数据处理管道,研究 dFMR1B55 突变体(雌雄蝇同时组成的群体)的社会网络。与野生型果蝇(w1118)相比,对dFMR1B55突变体进行的SNA分析表明,它们的活跃性低、网络中的连接较少、互动持续时间较长、有效传递信息的能力较低、可供选择的信息传递途径较少、它们实现的互动数量的可变性较高,而且果蝇倾向于停留在测试室的边界附近。这些观察到的变化表明,在 dFMR1B55 苍蝇中存在着特征性的品系依赖性社会网络,即通常所说的群体表型。最后,结合新的研究工具是果蝇SI研究的一种有价值的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信