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

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.

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

Programmed cell death inBradysia hygida (Diptera, Sciaridae) salivary glands presents apoptotic features

genesis ◽  
2004 ◽  
Vol 40 (1) ◽  
pp. 22-31 ◽  
Author(s):  
Cl�udio R. Simon ◽  
Jorge C. de Almeida
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Salivary Glands

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.

scholarly journals To die or not to die—a role for Fork head

2007 ◽  
Vol 176 (6) ◽  
pp. 737-739 ◽  
Author(s):  
Carl S. Thummel
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Salivary Glands ◽  
Precise Determination ◽  
Tissue Destruction ◽  
Fork Head ◽  
Massive Cell Death ◽  
Puparium Formation ◽  
Hormone Responses ◽  
And Function

The precise determination of when and where cells undergo programmed cell death is critical for normal development and tissue homeostasis. Cao et al. (2007; see p. 843 of this issue) report that the Fork head (Fkh) transcription factor, which is essential for the early development and function of the larval salivary glands in Drosophila melanogaster, also contributes to its demise. These authors show that fkh expression in the salivary glands is normally lost at puparium formation, which is ∼12 h before they undergo massive cell death triggered by the steroid hormone ecdysone, making room for their developing adult counterparts. The loss of Fkh eliminates its role in blocking cell death, allowing for subsequent ecdysone-induced reaper and head involution defective death activator expression and tissue destruction. This study provides new insights into the transcriptional regulation of programmed cell death and the mechanisms that underlie the precise spatial and temporal control of hormone responses during development.

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