Channel nuclear pore protein 54 directs sexual differentiation and neuronal wiring of female reproductive behaviors in Drosophila.
Channel nuclear pore protein 54 directs sexual differentiation and neuronal wiring of female reproductive behaviors in Drosophila.
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DOI:
10.1186/s12915-021-01154-6
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发表时间:
2021-10-20
期刊:
影响因子:
5.4
通讯作者:
Soller M
中科院分区:
文献类型:
--
作者:
Nallasivan MP;Haussmann IU;Civetta A;Soller M
Female reproductive behaviors and physiology change profoundly after mating. The control of pregnancy-associated changes in physiology and behaviors are largely hard-wired into the brain to guarantee reproductive success, yet the gene expression programs that direct neuronal differentiation and circuit wiring at the end of the sex determination pathway in response to mating are largely unknown. In Drosophila, the post-mating response induced by male-derived sex-peptide in females is a well-established model to elucidate how complex innate behaviors are hard-wired into the brain. Here, we use a genetic approach to further characterize the molecular and cellular architecture of the sex-peptide response in Drosophila females. Screening for mutations that affect the sensitivity to sex-peptide, we identified the channel nuclear pore protein Nup54 gene as an essential component for mediating the sex-peptide response, with viable mutant alleles leading to the inability of laying eggs and reducing receptivity upon sex-peptide exposure. Nup54 directs correct wiring of eight adult brain neurons that express pickpocket and are required for egg-laying, while additional channel Nups also mediate sexual differentiation. Consistent with links of Nups to speciation, the Nup54 promoter is a hot spot for rapid evolution and promoter variants alter nucleo-cytoplasmic shuttling. These results implicate nuclear pore functionality to neuronal wiring underlying the sex-peptide response and sexual differentiation as a response to sexual conflict arising from male-derived sex-peptide to direct the female post-mating response. The online version contains supplementary material available at 10.1186/s12915-021-01154-6.
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影响因子:
12.3
作者:
Haussmann IU;White K;Soller M
通讯作者:
Soller M
影响因子:
64.5
作者:
Asahina K;Watanabe K;Duistermars BJ;Hoopfer E;González CR;Eyjólfsdóttir EA;Perona P;Anderson DJ
通讯作者:
Anderson DJ
影响因子:
64.8
作者:
通讯作者:
--
影响因子:
9.2
作者:
Carvalho, GB;Kapahi, P;Benzer, S
通讯作者:
Benzer, S
影响因子:
14.9
作者:
Ilyin AA;Ryazansky SS;Doronin SA;Olenkina OM;Mikhaleva EA;Yakushev EY;Abramov YA;Belyakin SN;Ivankin AV;Pindyurin AV;Gvozdev VA;Klenov MS;Shevelyov YY
通讯作者:
Shevelyov YY