Targeted expression of p35 reveals a role for caspases in formation of the adult abdominal cuticle in Drosophila

Kester, Rachel S.; Nambu, John R.

doi:10.1387/ijdb.103109rk

Cited by 12 publications

(10 citation statements)

References 57 publications

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“…A large number of experimental studies have shown that caspase-3 plays an important role in the pathological process of myocardial and cerebral ischemia. It has attracted a great deal of attention, mainly for its role in the final common pathway of apoptosis (Yu et al, 2006;Kester and Nambu, 2011). The results of this study showed that the expression level of caspase-3 mRNA decreased significantly after the P35 protein was injected into the rats with ACI, which further confirms that the P35 protein has a certain inhibitory effect on the apoptosis pathway of brain tissue in rats following treatment.…”

Section: Discussionsupporting

confidence: 69%

Effect of baculovirus P35 protein on apoptosis in brain tissue of rats with acute cerebral infarction

Ji¹,

H²

2015

Genet. Mol. Res.

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ABSTRACT.We explored the effect of baculovirus P35 protein on apoptosis in the brain tissue of rats with acute cerebral infarction (ACI). A rat model of middle cerebral artery infarction was created. The rats were randomly divided into sham, model, and treatment groups. Baculovirus P35 protein was injected into the intracranial arteries of the treatment group rats. The rats in the model group were given an equal volume of phosphate-buffered saline. The rats were sacrificed after 72 h and the brain tissue was separated. The levels of caspase-3, Bcl-2, and Bax mRNA, the brain cell apoptosis index, and the infarct size were determined. After 72 h, the levels of caspase-3 and Bax mRNA in the model and treatment groups were significantly greater than in the sham group, and the levels of Bcl-2 mRNA were significantly smaller (P < 0.05). The levels of caspase-3 and Bax mRNA were significantly lower in the treatment group than in the model group, and the level of Bcl-2 mRNA was significantly greater (P < 0.05). Compared with the sham group, the brain tissue apoptosis index and the cerebral infarction area increased significantly in the model and treatment groups (P < 0.05). The brain tissue apoptosis index and cerebral infarction area in the treatment group were significantly lower than in the model group (P < 0.05). Baculovirus P35 protein can effectively inhibit brain cell apoptosis in rats with ACI. It delayed apoptosis and necrosis in subjects with ACI tissue and had a protective effect on brain tissue.

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Section: Discussionsupporting

confidence: 69%

Effect of baculovirus P35 protein on apoptosis in brain tissue of rats with acute cerebral infarction

Ji¹,

H²

2015

Genet. Mol. Res.

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“…To identify the photoreceptor defects were caused by inappropriate activation of apoptosis, we employed p35 to suppress apoptosis; P35 is cleaved and forms a thioester bond with the caspase active site, thereby causing irreversible inhibition of the caspase[42]. Furthermore, p35 effectively inhibits a broad range of active caspases and can block cell death [43]. We used the MARCM system to over-express p35 in the usp5 mutant clones.…”

Section: Resultsmentioning

confidence: 99%

Drosophila USP5 Controls the Activation of Apoptosis and the Jun N-Terminal Kinase Pathway during Eye Development

Fan

Huang

et al. 2014

PLoS ONE

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The Jun N-terminal kinase pathway plays an important role in inducing programmed cell death (apoptosis) and is activated in a variety of contexts. The deubiquitinating enzymes (DUBs) are proteases regulating the protein stability by ubiquitin-proteasome system. Here, for the first time, we report the phenotypes observed during eye development that are induced by deleting Drosophila USP5 gene, which encodes one of the USP subfamily of DUBs. usp5 mutants displayed defects in photoreceptor differentiation. Using genetic epistasis analysis and molecular markers, we show that most of these phenotypes are caused by the activation of apoptosis and JNK pathway. These data may provide a mechanistic model for understanding the mammalian usp5 gene.

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“…During metamorphosis, tergites and male genitalia development requires apoptosis [ 41 – 45 ]. Consistently, mutations in apoptotic genes such as Drice , or overexpression of the apoptosis inhibitors P35 or Diap1 in tergite and genitalia anlage, give rise to adult flies presenting cuticle midline and genitalia rotation defects [ 41 ]. To test if PGRP-LF mutant phenotypes are due to apoptosis inhibition in ectodermal anlage, we overexpressed P35 in PGRP-LF expression domain.…”

Section: Resultsmentioning

confidence: 99%

“…In contrast, neither loss-of function of PGRP-LF nor gain-of-function of IMD were able to activate pro-apoptotic Hid or Reaper transgenic reporter constructs in these tissues ( S10A–S10C Fig ). We could also showed that Diap1 ectopic expression using either a ubiquitous Gal4 ( Act5C Gal4 ) or PGRP-LF Gal4 drivers was sufficient to mimic both cuticle and genitalia defects ( S7C Fig ) [ 41 ]. Altogether these results show that by preventing IMD pathway activation in ectodermal derivatives, PGRP-LF is allowing normal cell death to occur and pupal development to proceed.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of a NF-κB/Diap1 Pathway by PGRP-LF Is Required for Proper Apoptosis during Drosophila Development

et al. 2017

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NF-κB pathways are key signaling cascades of the Drosophila innate immune response. One of them, the Immune Deficiency (IMD) pathway, is under a very tight negative control. Although molecular brakes exist at each step of this signaling module from ligand availability to transcriptional regulation, it remains unknown whether repressors act in the same cells or tissues and if not, what is rationale behind this spatial specificity. We show here that the negative regulator of IMD pathway PGRP-LF is epressed in ectodermal derivatives. We provide evidence that, in the absence of any immune elicitor, PGRP-LF loss-of-function mutants, display a constitutive NF-κB/IMD activation specifically in ectodermal tissues leading to genitalia and tergite malformations. In agreement with previous data showing that proper development of these structures requires induction of apoptosis, we show that ectopic activation of NF-κB/IMD signaling leads to apoptosis inhibition in both genitalia and tergite primordia. We demonstrate that NF-κB/IMD signaling antagonizes apoptosis by up-regulating expression of the anti-apoptotic protein Diap1. Altogether these results show that, in the complete absence of infection, the negative regulation of NF-κB/IMD pathway by PGRP-LF is crucial to ensure proper induction of apoptosis and consequently normal fly development. These results highlight that IMD pathway regulation is controlled independently in different tissues, probably reflecting the different roles of this signaling cascade in both developmental and immune processes.

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Targeted expression of p35 reveals a role for caspases in formation of the adult abdominal cuticle in Drosophila

Cited by 12 publications

References 57 publications

Effect of baculovirus P35 protein on apoptosis in brain tissue of rats with acute cerebral infarction

Effect of baculovirus P35 protein on apoptosis in brain tissue of rats with acute cerebral infarction

Drosophila USP5 Controls the Activation of Apoptosis and the Jun N-Terminal Kinase Pathway during Eye Development

Inhibition of a NF-κB/Diap1 Pathway by PGRP-LF Is Required for Proper Apoptosis during Drosophila Development

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