scholarly journals Autophagy and Apoptosis Coordinate Physiological Cell Death in Larval Salivary Glands ofApis mellifera(Hymenoptera: Apidae)

Autophagy ◽  
2007 ◽  
Vol 3 (5) ◽  
pp. 515-517 ◽  
Author(s):  
Elaine C.M. Silva-Zacarin
1991 ◽  
pp. 451-459
Author(s):  
R. A. Lockshin ◽  
Z. F. Zakeri ◽  
L. M. Yesner

2007 ◽  
Vol 236 (3) ◽  
pp. 880-885 ◽  
Author(s):  
V. Zuzarte-Luis ◽  
J.A. Montero ◽  
N. Torre-Perez ◽  
J.A. Garcia-Porrero ◽  
J.M. Hurle

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4673-4683 ◽  
Author(s):  
C. Jiang ◽  
E.H. Baehrecke ◽  
C.S. Thummel

During insect metamorphosis, pulses of the steroid hormone 20-hydroxyecdysone (ecdysone) direct the destruction of obsolete larval tissues and their replacement by tissues and structures that form the adult fly. We show here that larval midgut and salivary gland histolysis are stage-specific steroid-triggered programmed cell death responses. Dying larval midgut and salivary gland cell nuclei become permeable to the vital dye acridine orange and their DNA undergoes fragmentation, indicative of apoptosis. Furthermore, the histolysis of these tissues can be inhibited by ectopic expression of the baculovirus anti-apoptotic protein p35, implicating a role for caspases in the death response. Coordinate stage-specific induction of the Drosophila death genes reaper (rpr) and head involution defective (hid) immediately precedes the destruction of the larval midgut and salivary gland. In addition, the diap2 anti-cell death gene is repressed in larval salivary glands as rpr and hid are induced, suggesting that the death of this tissue is under both positive and negative regulation. Finally, diap2 is repressed by ecdysone in cultured salivary glands under the same conditions that induce rpr expression and trigger programmed cell death. These studies indicate that ecdysone directs the death of larval tissues via the precise stage- and tissue-specific regulation of key death effector genes.


1996 ◽  
Vol 4 (4-5) ◽  
pp. 341-353 ◽  
Author(s):  
Dorit Hanein ◽  
Anat Yarden ◽  
Helena Sabanay ◽  
Lia Addadi ◽  
Benjamin Geiger

1995 ◽  
Vol 15 (4) ◽  
pp. 299-311 ◽  
Author(s):  
Georg Häucker ◽  
David L. Vaux

2006 ◽  
Vol 926 (1) ◽  
pp. 83-89 ◽  
Author(s):  
PHILIPPE BOUILLET ◽  
DAVID C.S. HUANG ◽  
LORRAINE A. O'REILLY ◽  
HAMSA PUTHALAKATH ◽  
LIAM O'CONNOR ◽  
...  

1992 ◽  
Vol 12 (7) ◽  
pp. 3060-3069 ◽  
Author(s):  
D S Ucker ◽  
P S Obermiller ◽  
W Eckhart ◽  
J R Apgar ◽  
N A Berger ◽  
...  

We examined virally transformed murine fibroblast clones as targets for cytotoxic T lymphocyte (CTL)-triggered lysis and genome digestion. Strikingly, while all clones were essentially equivalent in the ability to be lysed, one clone, SV3T3-B2.1, failed to exhibit genome digestion associated with CTL attack. Other aspects of the physiological cell death process, including loss of adhesion and nuclear envelope breakdown (lamin phosphorylation and solubilization), were not altered in this clone. The absence of genome digestion associated with CTL-induced cell death correlated with the absence of endodeoxyribonuclease activity in the nuclei of that clone. Characterization of the activity affected identifies a calcium-dependent, DNase I-like endonuclease of approximately 40 kDa, normally present constitutively in all cell nuclei, as the enzyme responsible for genome digestion associated with CTL-mediated cell death. These observations indicate that neither genome digestion per se nor its consequences [such as activation of poly(ADP-ribose) polymerase] are essential for cell death resulting from the triggering of this cell suicide process.


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