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
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
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.
Animals, Cell Division, Centrioles/metabolism, Centrosome/metabolism, Cytoskeletal Proteins/metabolism, DNA Damage, Drosophila/metabolism, Drosophila Proteins/genetics, Microtubule-Organizing Center/metabolism, Microtubules/metabolism, Nuclear Proteins/metabolism, Stem Cells/metabolism
1740-1752
Zheng, Yiming
fc9ea2cd-c677-43b2-8ee9-77ce6333aa83
Mennella, Vito
43c60e29-c0a7-4ab8-8e5c-fcb59f70a28a
Marks, Steven
67c53dd0-bfda-4a1c-8f37-9fa65f5bcd1f
Wildonger, Jill
8cb30cff-fc69-48d8-b6dd-3231c74b599f
Elnagdi, Esraa
c9d7a3b0-412c-4c55-a054-a42a55da4df2
Agard, David
c0733eec-3b98-4a05-9cac-4a965769f5b1
Megraw, Timothy L
4238a01d-1391-4788-9628-c6d6cbd54477
1 June 2016
Zheng, Yiming
fc9ea2cd-c677-43b2-8ee9-77ce6333aa83
Mennella, Vito
43c60e29-c0a7-4ab8-8e5c-fcb59f70a28a
Marks, Steven
67c53dd0-bfda-4a1c-8f37-9fa65f5bcd1f
Wildonger, Jill
8cb30cff-fc69-48d8-b6dd-3231c74b599f
Elnagdi, Esraa
c9d7a3b0-412c-4c55-a054-a42a55da4df2
Agard, David
c0733eec-3b98-4a05-9cac-4a965769f5b1
Megraw, Timothy L
4238a01d-1391-4788-9628-c6d6cbd54477
Zheng, Yiming, Mennella, Vito, Marks, Steven, Wildonger, Jill, Elnagdi, Esraa, Agard, David and Megraw, Timothy 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, 27 (11), .
(doi:10.1091/mbc.E15-09-0655).
Abstract
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.
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e-pub ahead of print date: 6 April 2016
Published date: 1 June 2016
Keywords:
Animals, Cell Division, Centrioles/metabolism, Centrosome/metabolism, Cytoskeletal Proteins/metabolism, DNA Damage, Drosophila/metabolism, Drosophila Proteins/genetics, Microtubule-Organizing Center/metabolism, Microtubules/metabolism, Nuclear Proteins/metabolism, Stem Cells/metabolism
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Local EPrints ID: 434098
URI: http://eprints.soton.ac.uk/id/eprint/434098
ISSN: 1059-1524
PURE UUID: 990a46a5-e051-42c5-a869-7e49efa1e6e1
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Date deposited: 12 Sep 2019 16:30
Last modified: 16 Mar 2024 04:03
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Author:
Yiming Zheng
Author:
Steven Marks
Author:
Jill Wildonger
Author:
Esraa Elnagdi
Author:
David Agard
Author:
Timothy L Megraw
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