Steroid regulated programmed cell death during Drosophila metamorphosis

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4673-4683 ◽  
Author(s):  
C. Jiang ◽  
E.H. Baehrecke ◽  
C.S. Thummel
Keyword(s):  
Cell Death ◽  
Salivary Gland ◽  
Programmed Cell Death ◽  
Salivary Glands ◽  
Ectopic Expression ◽  
Salivary Gland Cell ◽  
Cell Nuclei ◽  
Larval Midgut ◽  
Insect Metamorphosis ◽  
Specific Regulation

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.

scholarly journals Down-regulation of inhibitor of apoptosis levels provides competence for steroid-triggered cell death

2007 ◽  
Vol 178 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Viravuth P. Yin ◽  
Carl S. Thummel ◽  
Arash Bashirullah
Keyword(s):  
Cell Death ◽  
Salivary Gland ◽  
Salivary Glands ◽  
Gland Cell ◽  
Inhibitor Of Apoptosis ◽  
Salivary Gland Cell ◽  
Creb Binding Protein ◽  
Down Regulation ◽  
Steroid Signaling ◽  
Necessary And Sufficient

A pulse of the steroid hormone ecdysone triggers the destruction of larval salivary glands during Drosophila metamorphosis through a transcriptional cascade that converges on reaper (rpr) and head involution defective (hid) induction, resulting in caspase activation and cell death. We identify the CREB binding protein (CBP) transcriptional cofactor as essential for salivary gland cell death. We show that CBP acts 1 d before the onset of metamorphosis in apparent response to a mid-third instar ecdysone pulse, when CBP is necessary and sufficient for down-regulation of the Drosophila inhibitor of apoptosis 1 (DIAP1). It is only after DIAP1 levels are reduced that salivary glands become competent to die through rpr/hid-mediated cell death. Before this time, high levels of DIAP1 block salivary gland cell death, even in the presence of ectopic rpr expression. This study shows that naturally occurring changes in inhibitor of apoptosis levels can be critical for regulating cell death during development. It also provides a molecular mechanism for the acquisition of competence in steroid signaling pathways.

Steroid regulation of autophagic programmed cell death during development

Development ◽  
2001 ◽  
Vol 128 (8) ◽  
pp. 1443-1455 ◽  
Author(s):  
C.Y. Lee ◽  
E.H. Baehrecke
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Salivary Glands ◽  
Plasma Membranes ◽  
Molecular Mechanisms ◽  
Gland Cell ◽  
Salivary Gland Cell ◽  
Membrane Breakdown ◽  
Nuclear Changes ◽  
Genetic Interval

Apoptosis and autophagy are morphologically distinct forms of programmed cell death. While autophagy occurs during the development of diverse organisms and has been implicated in tumorigenesis, little is known about the molecular mechanisms that regulate this type of cell death. Here we show that steroid-activated programmed cell death of Drosophila salivary glands occurs by autophagy. Expression of p35 prevents DNA fragmentation and partially inhibits changes in the cytosol and plasma membranes of dying salivary glands, suggesting that caspases are involved in autophagy. The steroid-regulated BR-C, E74A and E93 genes are required for salivary gland cell death. BR-C and E74A mutant salivary glands exhibit vacuole and plasma membrane breakdown, but E93 mutant salivary glands fail to exhibit these changes, indicating that E93 regulates early autophagic events. Expression of E93 in embryos is sufficient to induce cell death with many characteristics of apoptosis, but requires the H99 genetic interval that contains the rpr, hid and grim proapoptotic genes to induce nuclear changes diagnostic of apoptosis. In contrast, E93 expression is sufficient to induce the removal of cells by phagocytes in the absence of the H99 genes. These studies indicate that apoptosis and autophagy utilize some common regulatory mechanisms.

Interferon-γ induced cell death in a cultured human salivary gland cell line

1996 ◽  
Vol 167 (2) ◽  
pp. 297-304 ◽  
Author(s):  
Ava J. Wu ◽  
Zhi Jian Chen ◽  
Maria Tsokos ◽  
Brian C. O'Connell ◽  
Indu S. Ambudkar ◽  
...  
Keyword(s):  
Cell Death ◽  
Salivary Gland ◽  
Cell Line ◽  
Gland Cell ◽  
Interferon Γ ◽  
Salivary Gland Cell ◽  
Human Salivary Gland

scholarly journals A Steroid-Triggered Transcriptional Hierarchy Controls Salivary Gland Cell Death during Drosophila Metamorphosis

2000 ◽  
Vol 5 (3) ◽  
pp. 445-455 ◽  
Author(s):  
Changan Jiang ◽  
Anne-Françoise J. Lamblin ◽  
Hermann Steller ◽  
Carl S. Thummel
Keyword(s):  
Cell Death ◽  
Salivary Gland ◽  
Gland Cell ◽  
Salivary Gland Cell

scholarly journals IL-17 and CCR9+α4β7– Th17 Cells Promote Salivary Gland Inflammation, Dysfunction, and Cell Death in Sjögren’s Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Sun-Hee Hwang ◽  
Jin Seok Woo ◽  
Jeonghyeon Moon ◽  
SeungCheon Yang ◽  
Jin-Sil Park ◽  
...  
Keyword(s):  
Cell Death ◽  
Salivary Gland ◽  
B Cells ◽  
Salivary Glands ◽  
Sjögren's Syndrome ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Metabolic Abnormalities ◽  
T And B Cells ◽  
Sjögren‘S Syndrome

Previous studies have evaluated the roles of T and B cells in the pathogenesis of Sjögren’s syndrome (SS); however, their relationships with age-dependent and metabolic abnormalities remain unclear. We examined the impacts of changes associated with aging or metabolic abnormalities on populations of T and B cells and SS disease severity. We detected increased populations of IL-17-producing T and B cells, which regulate inflammation, in the salivary glands of NOD/ShiLtJ mice. Inflammation-induced human submandibular gland cell death, determined based on p-MLKL and RIPK3 expression levels, was significantly increased by IL-17 treatment. Among IL-17-expressing cells in the salivary gland, peripheral blood, and spleen, the α4β7 (gut-homing integrin)-negative population was significantly increased in aged NOD/ShiLtJ mice. The α4β7-positive population markedly increased in the intestines of aged NOD/ShiLtJ mice following retinoic acid (RA) treatment. A significant increase in α4β7-negative IL-17-expressing cells in salivary glands may be involved in the onset and progression of SS. These results suggest the potential therapeutic utility of RA in SS treatment.

Mechanisms of programmed cell death in the midgut and salivary glands from Bradysia hygida (Diptera: Sciaridae) during pupal–adult metamorphosis

2020 ◽  
Vol 44 (10) ◽  
pp. 1981-1990
Author(s):  
Thaylise Cassia Santos Przepiura ◽  
Aryelle M. Navarro ◽  
Rafaela Rosa Ribeiro ◽  
José R. Gomes ◽  
Karina V. Pitthan ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Salivary Glands ◽  
Bradysia Hygida

Programmed cell death in the larval salivary glands of Apis mellifera (Hymenoptera, Apidae)

2007 ◽  
Vol 32 (2) ◽  
pp. 309-328 ◽  
Author(s):  
E C M Silva-Zacarin ◽  
G A Tomaino ◽  
M R Brocheto-Braga ◽  
S R Taboga ◽  
R L M Silva de Moraes
Keyword(s):  
Cell Death ◽  
Apis Mellifera ◽  
Programmed Cell Death ◽  
Salivary Glands
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