The Drosophila retinoblastoma protein, Rbf1, induces a <i>debcl</i> and <i>drp1-</i>dependent mitochondrial apoptosis.

Clavier, Amandine; Ruby, Vincent; Rincheval-Arnold, Aurore; Mignotte, Bernard; Guénal, Isabelle

doi:10.1242/jcs.169896

Cited by 22 publications

(45 citation statements)

References 66 publications

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“…We have previously shown that the JNK pathway activation induced by rbf1 involved reactive oxygen species (ROS) in dying cells. 28 Many data report an activation of the JNK pathway depending on ROS. For example, in mammalian cells, the JNKKK ASK1 has been extensively characterized as a ROS-responsive kinase.…”

Section: Signals For Example the C-terminal Regions Of Slpr And Dtak1mentioning

confidence: 99%

Two different specific JNK activators are required to trigger apoptosis or compensatory proliferation in response to Rbf1 in Drosophila

et al. 2016

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The Jun Kinase (JNK) signaling pathway responds to diverse stimuli by appropriate and specific cellular responses such as apoptosis, differentiation or proliferation. The mechanisms that mediate this specificity remain largely unknown. The core of this signaling pathway, composed of a JNK protein and a JNK kinase (JNKK), can be activated by various putative JNKK kinases (JNKKK) which are themselves downstream of different adaptor proteins. A proposed hypothesis is that the JNK pathway specific response lies in the combination of a JNKKK and an adaptor protein upstream of the JNKK. We previously showed that the Drosophila homolog of pRb (Rbf1) and a mutant form of Rbf1 (Rbf1(D253A)) have JNK-dependent pro-apoptotic properties. Rbf1(D253A) is also able to induce a JNK-dependent abnormal proliferation. Here, we show that Rbf1-induced apoptosis triggers proliferation which depends on the JNK pathway activation. Taking advantage of these phenotypes, we investigated the JNK signaling involved in either Rbf1-induced apoptosis or in proliferation in response to Rbf1-induced apoptosis. We demonstrated that 2 different JNK pathways involving different adaptor proteins and kinases are involved in Rbf1-apoptosis (i.e. Rac1-dTak1-dMekk1-JNK pathway) and in proliferation in response to Rbf1-induced apoptosis (i.e., dTRAF1-Slipper-JNK pathway). Using a transient induction of rbf1, we show that Rbf1-induced apoptosis activates a compensatory proliferation mechanism which also depends on Slipper and dTRAF1. Thus, these 2 proteins seem to be key players of compensatory proliferation in Drosophila.

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Section: Signals For Example the C-terminal Regions Of Slpr And Dtak1mentioning

confidence: 99%

Two different specific JNK activators are required to trigger apoptosis or compensatory proliferation in response to Rbf1 in Drosophila

et al. 2016

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“…Altogether these observations show that that the survival of a cell is regulated by the interplay between RHG pro-apoptotic genes and the mitochondrial fusion machinery. Why mitochondrial localization of RHG pro-apoptotic proteins is significant for caspase activation, and what is the role of mitochondrial fragmentation and permeabilization remains unknown (Clavier, Ruby et al 2015, Clavier, Rincheval-Arnold et al 2016). …”

Section: Mechanisms Of Apoptosismentioning

confidence: 99%

Programmed cell death acts at different stages of Drosophila neurodevelopment to shape the central nervous system

2016

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Edited by Wilhelm JustNervous system development is a process that integrates cell proliferation, differentiation, and programmed cell death (PCD). PCD is an evolutionary conserved mechanism and a fundamental developmental process by which the final cell number in a nervous system is established. In vertebrates and invertebrates, PCD can be determined intrinsically by cell lineage and age, as well as extrinsically by nutritional, metabolic, and hormonal states. Drosophila has been an instrumental model for understanding how this mechanism is regulated. We review the role of PCD in Drosophila central nervous system development from neural progenitors to neurons, its molecular mechanism and function, how it is regulated and implemented, and how it ultimately shapes the fly central nervous system from the embryo to the adult. Finally, we discuss ideas that emerged while integrating this information.Keywords: apoptosis; Drosophila; neurodevelopment Apoptosis shapes Drosophila neural development from the emergence of neuroectoderm in the embryo to the eclosing adult. The earliest indication of programmed cell death (PCD) during neurodevelopment is at embryonic stages 11-12 [1-3], when the first neurons and epidermal cells die [4,5]. Neuronal apoptosis then increases dramatically peaking at embryonic stages 16-17, when the ventral nerve cord (VNC) condenses [3] and the embryo produces its first twitching movements [1]. Although the observed amount of neuronal death differs from embryo to embryo [5], symmetry in neuronal PCD is often observed between the right and left sides of a single embryo [1], indicating that both deterministic and 'random' processes participate in the selection of surviving neurons.Programmed cell death in Drosophila neural development comes in different flavors. It can be triggered by spatial, temporal, nutritional, hormonal, and metabolic signals; it can be regulated by Hox genes, Notch, and other signaling pathways; it can be mediated by one or more proapoptotic genes; and it can act at the stage of neural precursors, of newly born or of mature neurons/glia. What is clear is that dying is not trivial for a cell. Many layers of regulation exist that ensure

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“…En effet, Debcl et Buffy modulent la réponse apoptotique embryonnaire provoquée par irradiation [19]. Par ailleurs, Debcl joue un rôle crucial dans l'apoptose induite par Rbf1 alors que Buffy s'y oppose [17,21]. Ainsi, chez la drosophile, bien que le rôle des protéines de la famille Bcl-2 dans le contrôle de la mort cellulaire développementale apparaisse mineur, ces protéines semblent jouer un rôle majeur dans l'apoptose induite par un stress ou par l'homologue, chez la drosophile, de la protéine oncosuppressive pRb.…”

Section: Mort Cellulaireunclassified

“…Chez la drosophile, un lien existe entre les membres de la famille Bcl-2, la dynamique mitochondriale et la mort cellulaire. Nous avons récemment montré que Debcl et Drp1 pouvaient interagir entre eux et que Buffy inhibait cette interaction (Figure 2) [21]. De façon intéressante, Debcl module la localisation mitochondriale de Drp1 au cours de l'apoptose et l'apoptose induite par Debcl, nécessite Drp1 et implique une fragmentation mitochondriale.…”

Section: Mort Cellulaireunclassified

“…De façon intéressante, Debcl module la localisation mitochondriale de Drp1 au cours de l'apoptose et l'apoptose induite par Debcl, nécessite Drp1 et implique une fragmentation mitochondriale. Cette alté-ration de la dynamique mitochondriale induite par Debcl déclenche une accumulation de ROS qui sont eux-mêmes nécessaires au déclenchement de l'apoptose [21]. Ces résultats permettent donc d'identifier un mécanisme par lequel Debcl peut contrôler l'apoptose.…”

Section: Mort Cellulaireunclassified

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Lecome-backde la mitochondrie dans l’apoptose chez la drosophile

Clavier¹,

Rincheval-Arnold²,

Mignotte³

et al. 2016

Med Sci (Paris)

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The Drosophila retinoblastoma protein, Rbf1, induces a debcl and drp1-dependent mitochondrial apoptosis.

Cited by 22 publications

References 66 publications

Two different specific JNK activators are required to trigger apoptosis or compensatory proliferation in response to Rbf1 in Drosophila

Two different specific JNK activators are required to trigger apoptosis or compensatory proliferation in response to Rbf1 in Drosophila

Programmed cell death acts at different stages of Drosophila neurodevelopment to shape the central nervous system

Lecome-backde la mitochondrie dans l’apoptose chez la drosophile

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