Regulation and execution of apoptosis duringDrosophila development

Bangs, Peter Lawrence; White, Kristin

doi:10.1002/(sici)1097-0177(200005)218:1<68::aid-dvdy6>3.0.co;2-9

Cited by 74 publications

(39 citation statements)

References 82 publications

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“…15 Several non-exclusive models could explain how multiple RHG genes are activated to initiate the timely death of cells. Individual RHG genes could be turned on or off independently, by regulatory sequences specific for each gene.…”

Section: Discussionmentioning

confidence: 99%

“…14 RHG activity is controlled mainly at the level of transcription. 15 In the doomed cells, the transcription of multiple RHG genes is initiated 1-2 h before the cells begin to show signs of cell death. [16][17][18][19] Importantly, the RHG genes are clustered together in the genome, and there is evidence that shared cisregulatory regions control the transcription of more than one RHG gene.…”

mentioning

confidence: 99%

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Neural stem cell progeny regulate stem cell death in a Notch and Hox dependent manner

et al. 2015

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Neural stem cell progeny regulate stem cell death in a Notch and Hox dependent manner

et al. 2015

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“…Data presented in this report suggest that this increase is prevented by intrathymic signals, which are triggered by the increased size of the cells and which elicit events aimed at maintaining the thymic cell mass constant. These signals may limit the number of thymocytes by any of three non-mutually exclusive mechanisms: (i) they may increase apoptosis (18)(19)(20); (ii) they may reset the minimal size checkpoint so that a larger cell size is required to permit the transition from G 1 to S (7-11); or (iii) they may limit the number of cell divisions T cell precursors may undergo during maturation (35)(36)(37)(38). MyrAkt exerts a strong anti-apoptotic effect (1) which makes the first possibility unlikely.…”

Section: Discussionmentioning

confidence: 99%

“…Multicellular organisms and their organs sense either the total cell mass (11,12) or the total cell number (13,14) to initiate homeostatic signals that are superimposed on the intrinsic cellular signals regulating cell cycle progression (15)(16)(17) or cell death (18)(19)(20). The purpose of these signals is to couple the total cell number or the total cell mass in a given organ or organism with the pathways that regulate cellular proliferation and death.…”

mentioning

confidence: 99%

Tumor induction by an Lck-MyrAkt transgene is delayed by mechanisms controlling the size of the thymus

Malstrom

Tili

Kappes

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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Transgenic mice expressing MyrAkt from a proximal Lck promoter construct develop thymomas at an early age, whereas transgenic mice expressing constitutively active Lck-AktE40K develop primarily tumors of the peripheral lymphoid organs later in life. The thymus of 6-to 8-week-old MyrAkt transgenic mice is normal in size but contains fewer, larger cells than the thymus of nontransgenic control and AktE40K transgenic mice. Earlier studies had shown that cell size and cell cycle are coordinately regulated. On the basis of this finding, and our observations that the oncogenic potential of Akt correlates with its effect on cell size, we hypothesized that mechanisms aimed at maintaining the size of the thymus dissociate cell size and cell cycle regulation by blocking MyrAkt-promoted G1 progression and that failure of these mechanisms may promote cell proliferation resulting in an enlarged neoplastic thymus. To address this hypothesis, we examined the cell cycle distribution of freshly isolated and cultured thymocytes from transgenic and nontransgenic control mice. The results showed that although neither transgene alters cell cycle distribution in situ, the MyrAkt transgene promotes G1 progression in culture. Freshly isolated MyrAkt thymocytes express high levels of cyclins D2 and E and cdk4 but lower than normal levels of cyclin D3 and cdk2. Cultured thymocytes from MyrAkt transgenic mice, on the other hand, express high levels of cyclin D3, suggesting that the hypothesized organ size control mechanisms may down-regulate the expression of this molecule. Primary tumor cells, similar to MyrAkt thymocytes in culture, express high levels of cyclin D3. These findings support the hypothesis that tumor induction is caused by the failure of organ size control mechanisms to downregulate cyclin D3 and to block MyrAkt-promoted G1 progression.

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“…In Drosophila, the induction of apoptosis requires the activity of the closely linked proapoptotic genes reaper (rpr), head involution defective (hid) and grim, which induce cell death by activating a family of executing proteases known as caspases. 1,2 Cell death is suppressed by the Drosophila inhibitor of apoptosis protein I (DIAPI), which directly inhibits caspase activity and promotes their ubiquitination and subsequent degradation. 3 Recent findings suggest that Rprmediated DIAP1 inhibition leads to an induction of Jun Nterminal kinase (JNK) signalling, which was shown to induce apoptosis during imaginal disc development in Drosophila.…”

Section: Introductionmentioning

confidence: 99%

Mutations in rugose promote cell type-specific apoptosis in the Drosophila eye

Wech

Nagel

2005

Cell Death Differ

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rugose (rg) encodes an A kinase anchor protein and was isolated as a genetic interactor of the Notch and epidermal growth factor receptor (EGFR) pathways during eye development in Drosophila. rg mutants display a small, rough eye phenotype primarily caused by the loss of cone cells. Here we show that the basis of this phenotype is cell type-specific apoptosis rather than transformation and hence can be rescued by reduction of proapoptotic signals. Moreover, a nearly complete rescue is observed by an increased Notch signal suggesting an antiapoptotic function of Notch in this developmental context. Cone cell loss in rg mutants is accompanied by enhanced Jun N-terminal kinase activity and, concomitantly, by a reduction of EGFR signalling activity. Together, these findings support the idea that rg plays an important role in the integration of different signals required for the exact regulation of cone cell development and survival.

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Regulation and execution of apoptosis duringDrosophila development

Cited by 74 publications

References 82 publications

Neural stem cell progeny regulate stem cell death in a Notch and Hox dependent manner

Neural stem cell progeny regulate stem cell death in a Notch and Hox dependent manner

Tumor induction by an Lck-MyrAkt transgene is delayed by mechanisms controlling the size of the thymus

Mutations in rugose promote cell type-specific apoptosis in the Drosophila eye

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