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Seckel syndrome and centrosomal protein Ninein localizes asymmetrically to stem cell centrosomes but is not required for normal development, behavior, or DNA damage response in Drosophila.

Title: The Seckel syndrome and centrosomal protein Ninein localizes asymmetrically to stem cell centrosomes but is not required for normal development, behavior, or DNA damage response in Drosophila.
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Name(s): Zheng, Yiming, author
Mennella, Vito, author
Marks, Steven, author
Wildonger, Jill, author
Elnagdi, Esraa, author
Agard, David, author
Megraw, Timothy L, author
Type of Resource: text
Genre: Journal Article
Text
Date Issued: 2016-06-01
Physical Form: computer
online resource
Extent: 1 online resource
Language(s): English
Abstract/Description: Ninein (Nin) is a centrosomal protein whose gene is mutated in Seckel syndrome (SCKL, MIM 210600), an inherited recessive disease that results in primordial dwarfism, cognitive deficiencies, and increased sensitivity to genotoxic stress. Nin regulates neural stem cell self-renewal, interkinetic nuclear migration, and microtubule assembly in mammals. Nin is evolutionarily conserved, yet its role in cell division and development has not been investigated in a model organism. Here we characterize the single Nin orthologue in Drosophila Drosophila Nin localizes to the periphery of the centrosome but not at centriolar structures as in mammals. However, Nin shares the property of its mammalian orthologue of promoting microtubule assembly. In neural and germline stem cells, Nin localizes asymmetrically to the younger (daughter) centrosome, yet it is not required for the asymmetric division of stem cells. In wing epithelia and muscle, Nin localizes to noncentrosomal microtubule-organizing centers. Surprisingly, loss of nin expression from a nin mutant does not significantly affect embryonic and brain development, fertility, or locomotor performance of mutant flies or their survival upon exposure to DNA-damaging agents. Although it is not essential, our data suggest that Nin plays a supportive role in centrosomal and extracentrosomal microtubule organization and asymmetric stem cell division.
Identifier: FSU_pmch_27053665 (IID), 10.1091/mbc.E15-09-0655 (DOI), PMC4884065 (PMCID), 27053665 (RID), 27053665 (EID), mbc.E15-09-0655 (PII)
Grant Number: R01 GM068758
Publication Note: This NIH-funded author manuscript originally appeared in PubMed Central at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4884065.
Persistent Link to This Record: http://purl.flvc.org/fsu/fd/FSU_pmch_27053665
Owner Institution: FSU
Is Part Of: Molecular biology of the cell.
1939-4586
Issue: iss. 11, vol. 27

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Zheng, Y., Mennella, V., Marks, S., Wildonger, J., Elnagdi, E., Agard, D., & Megraw, T. L. (2016). The Seckel syndrome and centrosomal protein Ninein localizes asymmetrically to stem cell centrosomes but is not required for normal development, behavior, or DNA damage response in Drosophila. Molecular Biology Of The Cell. Retrieved from http://purl.flvc.org/fsu/fd/FSU_pmch_27053665