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Increase of 30K protein in identified motoneurons by hemolymph results in inhibition of programmed cell death in silkworm, Bombyx mori (Lepidoptera, Bombycidae)

Authors
Song, Hwa YoungKim, Mi YoungKim, Bo YongPark, Sun WhanSung, Dong KyoungKang, Pil DonPark, CheolinJeon, Soung HooLee, Bong Hee
Issue Date
5월-2012
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
Programmed cell death; Motoneuron; Hemolymph; Recombinant 30K protein; Ecdysone; Ecdysone receptor
Citation
JOURNAL OF INSECT PHYSIOLOGY, v.58, no.5, pp.756 - 762
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF INSECT PHYSIOLOGY
Volume
58
Number
5
Start Page
756
End Page
762
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/108571
DOI
10.1016/j.jinsphys.2012.03.004
ISSN
0022-1910
Abstract
This study demonstrates that a 30K protein was gradually synthesized in primary-cultured motoneurons from the accessory planta retractor (APR) of the 6th abdominal ganglion (APR6) in silkworm ventral ganglia through stimulation of hemolymph. An increase in 30K protein synthesis resulted in an inhibition of programmed cell death (PCD) of APR6 motoneurons. The 30K protein was gradually synthesized from the 30Kc6 gene of identified APR6s in day-6 4th instars to day-9 5th instar larvae, but synthesis of the 30K protein ceased in isolated APR6s of day-1 pupa, which normally begin to undergo PCD. When pupal APR6s were treated with larval hemolymph, however, the 30K protein was synthesized suggesting the existence of an anti-PCD factor in the larval hemolymph. An increase of 30K protein within the APR6s was confirmed by antiserum made against the recombinant 30K protein that originated from the APR 30Kc6 gene. Larval APR6, in which PCD was induced with 20-hydroxyecdysone (20E) added to the primary culture, exhibited some PCD characteristics of shrinkage of cell bodies, axonal fragmentation and loss of mitochondrial function. These results provide new insights on the survival or PCD of insect motoneurons through stimulation of hemolymph. (C) 2012 Elsevier Ltd. All rights reserved.
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