@article {69444,
	title = {The kinase ZYG-1 phosphorylates the cartwheel protein SAS-5 to drive centriole assembly in C. elegans},
	journal = {EMBO Rep},
	year = {2024},
	month = {2024 May 14},
	abstract = {<p>Centrioles organize centrosomes, the cell{\textquoteright}s primary microtubule-organizing centers (MTOCs). Centrioles double in number each cell cycle, and mis-regulation of this process is linked to diseases such as cancer and microcephaly. In C. elegans, centriole assembly is controlled by the Plk4 related-kinase ZYG-1, which recruits the SAS-5-SAS-6 complex. While the kinase activity of ZYG-1 is required for centriole assembly, how it functions has not been established. Here we report that ZYG-1 physically interacts with and phosphorylates SAS-5 on 17 conserved serine and threonine residues in vitro. Mutational scanning reveals that serine 10 and serines 331/338/340 are indispensable for proper centriole assembly. Embryos expressing SAS-5 exhibit centriole assembly failure, while those expressing SAS-5 possess extra centrioles. We show that in the absence of serine 10 phosphorylation, the SAS-5-SAS-6 complex is recruited to centrioles, but is not stably incorporated, possibly due to a failure to coordinately recruit the microtubule-binding protein SAS-4. Our work defines the critical role of phosphorylation during centriole assembly and reveals that ZYG-1 might play a role in preventing the formation of excess centrioles.</p>
},
	issn = {1469-3178},
	doi = {10.1038/s44319-024-00157-y},
	author = {Sankaralingam, Prabhu and Wang, Shaohe and Liu, Yan and Oegema, Karen F and O{\textquoteright}Connell, Kevin F}
}
@article {65203,
	title = {Drosulfakinin signaling in fruitless circuitry antagonizes P1 neurons to regulate sexual arousal in Drosophila.},
	journal = {Nature Communications},
	volume = {10},
	year = {2019},
	month = {2019 Oct 18},
	pages = {4770},
	abstract = {<p>Animals perform or terminate particular behaviors by integrating external cues and internal states through neural circuits. Identifying neural substrates and their molecular modulators promoting or inhibiting animal behaviors are key steps to understand how neural circuits control behaviors. Here, we identify the Cholecystokinin-like peptide Drosulfakinin (DSK) that functions at single-neuron resolution to suppress male sexual behavior in Drosophila. We found that Dsk neurons physiologically interact with male-specific P1 neurons, part of a command center for male sexual behaviors, and function oppositely to regulate multiple arousal-related behaviors including sex, sleep and spontaneous walking. We further found that the DSK-2 peptide functions through its receptor CCKLR-17D3 to suppress sexual behaviors in flies. Such a neuropeptide circuit largely overlaps with the fruitless-expressing neural circuit that governs most aspects of male sexual behaviors. Thus DSK/CCKLR signaling in the sex circuitry functions antagonistically with P1 neurons to balance arousal levels and modulate sexual behaviors.</p>
},
	issn = {2041-1723},
	doi = {10.1038/s41467-019-12758-6},
	author = {Wu, Shunfan and Guo, Chao and Zhao, Huan and Sun, Mengshi and Chen, Jie and Han, Caihong and Peng, Qionglin and Qiao, Huanhuan and Peng, Ping and Liu, Yan and Luo, Shengzhan D and Pan, Yufeng}
}
