Tango7 regulates cortical activity of caspases during reaper-triggered changes in tissue elasticity

Kang, Yunsik; Neuman, Sarah D.; Bashirullah, Arash

doi:10.1038/s41467-017-00693-3

Cited by 34 publications

(56 citation statements)

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“…In other words, cells below the threshold may have caspase activity but remain alive. A recent study in salivary glands suggests a mechanism for remaining below the threshold [ 72 ]. During Drosophila metamorphosis, salivary glands experience first a non-lethal dose of caspase activity, which cleaves cortical F-actin to alter cell morphology.…”

Section: Key Remaining Questionsmentioning

confidence: 99%

“…This is followed by a later, higher dose that leads to cell death and dissolution of the gland. The two doses are controlled by hormone-induced waves of transcriptional factor activity that modulates the transcription of IAP antagonist Rpr, low for the first non-lethal dose and higher for the later lethal dose [ 72 ]. Related, in mouse ESCs, the level and speed of cytochrome c release from the mitochondria is suggested to define the level of caspase-3 activation [ 73 ].…”

Section: Key Remaining Questionsmentioning

confidence: 99%

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Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different

2018

Open Biol.

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The ability to regenerate is a fundamental requirement for tissue homeostasis. Regeneration draws on three sources of cells. First and best-studied are dedicated stem/progenitor cells. Second, existing cells may proliferate to compensate for the lost cells of the same type. Third, a different cell type may change fate to compensate for the lost cells. This review focuses on regeneration of the third type and will discuss the contributions by post-transcriptional mechanisms including the emerging evidence for cell-autonomous and non-lethal roles of cell death pathways.

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Section: Key Remaining Questionsmentioning

confidence: 99%

Section: Key Remaining Questionsmentioning

confidence: 99%

Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different

2018

Open Biol.

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“…The initiator caspases form dimers and then are autocleaved in an apoptosome, resulting in activated initiator caspases that can then activate downstream effector caspases, again through proteolytical cleavage. Activated effector caspases can cleave the cellular components, leading to eventual apoptosis [7].…”

Section: Introductionmentioning

confidence: 99%

Pro-Apoptotic Function Analysis of the Reaper Homologue IBM1 in Spodoptera frugiperda

Shu

Zhang

Veeran

et al. 2020

IJMS

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As an important type of programmed cell death, apoptosis plays a critical role in lepidopteran insects in response to various internal and external stresses. It is controlled by a network of genes such as those encoding the inhibitor of apoptosis proteins. However, there are few studies on apoptosis-related genes in Spodoptera frugiperda. In this study, an orthologue to the Drosophila reaper gene, named Sf-IBM1, was identified from S. frugiperda, and a full-length sequence was obtained by reverse transcription polymerase chain reaction (RT-PCR) and rapid amplification of cDNA ends PCR (RACE-PCR). The expression pattern of Sf-IBM1 was determined in different developmental stages and various tissues. Apoptotic stimuli including azadirachtin, camptothecin, and ultraviolet radiation (UV) induced the expression of Sf-IBM1 at both transcript and protein levels. Overexpression of Sf-IBM1 induced apoptosis in Sf9 cells, and the Sf-IBM1 protein was localized in mitochondria. The apoptosis induced by Sf-IBM1 could be blocked by the caspase universal inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone (Z-VAD-FMK) and Sf-IAP1. Our results provide valuable information that should contribute to a better understanding of the molecular events that lead to apoptosis in lepidopterans.Apoptosis is inhibited by the inhibitor of apoptosis proteins (IAPs), which are endogenous caspase inhibitors and were originally identified in the genomes of lepidopteran baculoviruses [8]. Numerous IAPs have been identified from various insects and have been demonstrated to be the negative regulators of apoptosis [9]. For example, the Drosophila IAP1 (DIAP1) can enhance ubiquitylation and inhibit the activity of Dronc both in vitro and in vivo [10]. Co-expression of Bm-IAP1 in Bombyx mori suppresses apoptosis induced by overexpression of Bm-Dronc in BM-N cells [9]. IAPs contain two functional domains, the baculoviral IAP repeat (BIR) domain and the Really Interesting New Gene (RING) domain. The IBR domain may be involved in direct inhibition of apoptosis, whereas the RING domain may take part in protein-protein interactions. IAPs can bind to both initiator and effector caspases directly and degrade activated caspases through the E3 ubiquitin ligase activity, resulting in inhibition of apoptosis [11].The anti-apoptotic function of IAPs can be neutralized by IAP antagonists. IAP antagonists are the proteins containing the evolutionarily conserved IAP binding motif (IBM), which consists of several amino acids at the N-terminal [12]. In Drosophila, five RHG (Rpr, Hid, Grim) family proteins including Reaper, Hid, Grim, Sickle, and Jafrac2 have been identified, each with an IBM motif in the N-terminus and identified as the IAP antagonists [13]. Similarly, two IAP antagonists, Smac/Diablo and HtrA2/Omi have also been identified in mammals [14]. IAP antagonists compete with caspases by binding to the BIR domains of IAPs with different affinities via IBM directly [15]. Besides, the IAP antagonists can also function as positive regulato...

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“…Nascent granules mature via homotypic fusion, reaching a terminal size of 5-8 µm in diameter (Reynolds et al, 2019;Neuman and Bashirullah, 2018;Niemeyer and Schwarz, 2000). Mature granules then undergo steroid hormone-dependent exocytosis beginning about 4 h before the onset of metamorphosis (Kang et al, 2017;Biyasheva et al, 2001). After exocytosis, mucins are expelled out of the lumen of the salivary gland and onto the surface of the animal, allowing the prepupa to adhere to a surface during metamorphosis.…”

Section: Introductionmentioning

confidence: 99%

Mistargeting of secretory cargo in retromer-deficient cells

Neuman

Terry

Selegue

et al. 2020

Preprint

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ABSTRACTIntracellular trafficking is a basic and essential cellular function required for delivery of proteins to the appropriate subcellular destination; this process is especially demanding in professional secretory cells, which synthesize and secrete massive quantities of cargo proteins via regulated exocytosis. The Drosophila larval salivary glands are professional secretory cells that synthesize and secrete mucin proteins at the onset of metamorphosis. Using the larval salivary glands as a model system, we have identified a role for the highly conserved retromer complex in trafficking of secretory granule membrane proteins. We demonstrate that retromer-dependent trafficking via endosomal tubules is induced at the onset of secretory granule biogenesis, and that recycling via endosomal tubules is required for delivery of essential secretory granule membrane proteins to nascent granules. Without retromer function, nascent granules do not contain the proper membrane proteins; as a result, cargo from these defective granules is mistargeted to Rab7-positive endosomes, where it progressively accumulates to generate dramatically enlarged endosomes. Retromer complex dysfunction is strongly associated with Alzheimer’s disease, characterized by accumulation of amyloid β (Aβ). We show that amyloid precursor protein (APP) undergoes regulated exocytosis and accumulates within enlarged endosomes in retromer-deficient cells. These results highlight recycling of secretory granule membrane proteins as a critical step during secretory granule maturation and provide new insights into our understanding of retromer complex function in secretory cells. Our data also suggests that misrouting of secretory cargo, including APP, may contribute to the progressive nature of neurodegenerative disease.SUMMARY STATEMENTRetromer complex dysfunction is implicated in neurodegeneration. Here the authors show a new role for the retromer complex in recycling of secretory membrane and cargo proteins during regulated exocytosis.

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Tango7 regulates cortical activity of caspases during reaper-triggered changes in tissue elasticity

Cited by 34 publications

References 62 publications

Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different

Cellular plasticity, caspases and autophagy; that which does not kill us, well, makes us different

Pro-Apoptotic Function Analysis of the Reaper Homologue IBM1 in Spodoptera frugiperda

Mistargeting of secretory cargo in retromer-deficient cells

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