scholarly journals Essential role of grim-led programmed cell death for the establishment of corazonin-producing peptidergic nervous system during embryogenesis and metamorphosis in Drosophila melanogaster

Biology Open ◽  
2013 ◽  
Vol 2 (3) ◽  
pp. 283-294 ◽  
Author(s):  
G. Lee ◽  
R. Sehgal ◽  
Z. Wang ◽  
S. Nair ◽  
K. Kikuno ◽  
...  
2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S96-S97
Author(s):  
Andrew M Pickering

Abstract Cognitive function declines with age throughout the animal kingdom and increasing evidence shows that disruption of the proteasome system contributes to this decline. The proteasome has important roles in multiple aspects of the nervous system, including synapse function and plasticity, as well as preventing cell death and senescence. We report that augmentation of proteasome function, using overexpression of the proteasome β5 subunit, enhances proteasome assembly and function. Significantly, we go on to show neuronal-specific proteasome augmentation slows age-related declines in measures of learning, memory, and circadian rhythmicity. Surprisingly neuronal specific proteasome augmentation of proteasome function also produces a robust increase of lifespan in Drosophila melanogaster. Our findings appear specific to the nervous system; ubiquitous proteasome overexpression increases oxidative stress resistance but does not impact lifespan and is detrimental to some healthspan measures. These findings demonstrate a key role of the proteasome system in brain aging.


Development ◽  
2007 ◽  
Vol 134 (1) ◽  
pp. 105-116 ◽  
Author(s):  
A. Rogulja-Ortmann ◽  
K. Luer ◽  
J. Seibert ◽  
C. Rickert ◽  
G. M. Technau

2007 ◽  
Vol 12 (5) ◽  
pp. 807-816 ◽  
Author(s):  
Gaurav Goyal ◽  
Brennan Fell ◽  
Apurva Sarin ◽  
Richard J. Youle ◽  
V. Sriram

Nature ◽  
2001 ◽  
Vol 410 (6828) ◽  
pp. 549-554 ◽  
Author(s):  
Nicholas Joza ◽  
Santos A. Susin ◽  
Eric Daugas ◽  
William L. Stanford ◽  
Sarah K. Cho ◽  
...  

2008 ◽  
Vol 36 (5) ◽  
pp. 813-817 ◽  
Author(s):  
Patricia Boya ◽  
María Angeles Mellén ◽  
Enrique J. de la Rosa

Programmed cell death, together with proliferation and differentiation, is an essential process during the development of the nervous system. During neurogenesis, neurons and glia are generated in large numbers and, subsequently, they die in a process that depends on trophic signalling that refines the cytoarchitecture and connectivity of the nervous system. In addition, programmed cell death also affects proliferating neuroepithelial cells and recently differentiated neuroblasts. Autophagy is a lysosomal degradative pathway that allows the recycling of cell constituents, and seems to be able to play a dual role. It may serve to protect the cell by preventing the accumulation of deleterious products and organelles and supplying energy and amino acids. On the other hand, it has been considered a type of cell death. The role of autophagy during development is little characterized. The retina provides an excellent model system to study autophagy in the context of neural development, and to establish its relationship with proliferation, differentiation and cell death. In the present review, we summarize recent findings showing that autophagy contributes to the development of the nervous system by providing energy for cell corpse removal after physiological cell death, a process associated with retinal neurogenesis.


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