An essential function of AP-1 heterodimers in Drosophila development

Ciapponi, Laura; Bohmann, Dirk

doi:10.1016/s0925-4773(02)00093-x

Cited by 23 publications

(22 citation statements)

References 22 publications

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“…Known interaction with AP-1 in other tissues: We picked candidates that have been shown to influence AP-1 function in other cell types and physiological processes but not in neurons. For instance, we chose genes that interact with AP-1 to regulate embryonic dorsal closure (Riesgo-Escovar and Hafen 1997;Ciapponi and Bohmann 2002;Jacinto et al 2002). c. Strength of phenotype and isolation of multiple alleles:…”

Section: Resultsmentioning

confidence: 99%

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Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggyas a Regulator of AP-1-Dependent Developmental Plasticity

et al. 2008

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AP-1, an immediate-early transcription factor comprising heterodimers of the Fos and Jun proteins, has been shown in several animal models, including Drosophila, to control neuronal development and plasticity. In spite of this important role, very little is known about additional proteins that regulate, cooperate with, or are downstream targets of AP-1 in neurons. Here, we outline results from an overexpression/misexpression screen in Drosophila to identify potential regulators of AP-1 function at third instar larval neuromuscular junction (NMJ) synapses. First, we utilize .4000 enhancer and promoter (EP) and EPgy2 lines to screen a large subset of Drosophila genes for their ability to modify an AP-1-dependent eye-growth phenotype. Of 303 initially identified genes, we use a set of selection criteria to arrive at 25 prioritized genes from the resulting collection of putative interactors. Of these, perturbations in 13 genes result in synaptic phenotypes. Finally, we show that one candidate, the GSK-3b-kinase homolog, shaggy, negatively influences AP-1-dependent synaptic growth, by modulating the Jun-Nterminal kinase pathway, and also regulates presynaptic neurotransmitter release at the larval neuromuscular junction. Other candidates identified in this screen provide a useful starting point to investigate genes that interact with AP-1 in vivo to regulate neuronal development and plasticity.

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Section: Resultsmentioning

confidence: 99%

“…For instance, Fos regulates G2/M transition in dividing ommatidia and also controls cell survival and growth (Ciapponi and Bohmann 2002;Hyun et al 2006). More pertinently, studies using the motor synapse demonstrate that AP-1 positively regulates growth and presynaptic neurotransmitter release (Sanyal et al 2002;Collins et al 2006).…”

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confidence: 99%

Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggyas a Regulator of AP-1-Dependent Developmental Plasticity

et al. 2008

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“…It is important to note that c-Jun typically heterodimerizes with c-Fos, and together they constitute a member of the AP-1 family of transcription factors [69,70]. Thus, it will be important to determine whether PAGE4 interacts with c-Jun alone or with the Jun/Fos heterodimer and how this interaction could affect its ability to potentiate AP-1 transactivation.…”

Section: Discussionmentioning

confidence: 99%

The Stress-response protein prostate-associated gene 4, interacts with c-Jun and potentiates its transactivation

Rajagopalan

Qiu

Mooney

et al. 2014

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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The Cancer/Testis Antigen (CTA), Prostate-associated Gene 4 (PAGE4), is a stress-response protein that is upregulated in prostate cancer (PCa) especially in precursor lesions that result from inflammatory stress. In cells under stress, translocation of PAGE4 to mitochondria increases while production of reactive oxygen species decreases. Furthermore, PAGE4 is also upregulated in human fetal prostate, underscoring its potential role in development. However, the proteins that interact with PAGE4 and the mechanisms underlying its pleiotropic functions in prostatic development and disease remain unknown. Here, we identified c-Jun as a PAGE4 interacting partner. We show that both PAGE4 and c-Jun are overexpressed in the human fetal prostate; and in cell-based assays, PAGE4 robustly potentiates c-Jun transactivation. Single-molecule Förster resonance energy transfer experiments indicate that upon binding to c-Jun, PAGE4 undergoes conformational changes. However, no interaction is observed in presence of BSA or unilamellar vesicles containing the mitochondrial inner membrane diphosphatidylglycerol lipid marker cardiolipin. Together, our data indicate that PAGE4 specifically interacts with c-Jun and that, conformational dynamics may account for its observed pleiotropic functions. To our knowledge, this is the first report demonstrating crosstalk between a CTA and a proto-oncogene. Disrupting PAGE4/c-Jun interactions using small molecules may represent a novel therapeutic strategy for PCa.

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“…These complexities contribute to functional complementation when only a single AP-1 gene is knocked out (Jochum et al, 2001). By contrast, model organisms with reduced genetic redundancy allow functional analysis of AP-1 dimers and their corresponding target genes, as shown by studies in Drosophila (Kockel et al, 2001;Ciapponi and Bohmann, 2002).…”

Section: Ap-1 Dimerization In Transcriptional Regulation Ofmentioning

confidence: 99%

Caenorhabditis elegans FOS-1 and JUN-1 Regulateplc-1Expression in the Spermatheca to Control Ovulation

Hiatt

Duren

Shyu

et al. 2009

MBoC

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Fos and Jun are components of activator protein-1 (AP-1) and play crucial roles in the regulation of many cellular, developmental, and physiological processes. Caenorhabditis elegans fos-1 has been shown to act in uterine and vulval development. Here, we provide evidence that C. elegans fos-1 and jun-1 control ovulation, a tightly regulated rhythmic program in animals. Knockdown of fos-1 or jun-1 blocks dilation of the distal spermathecal valve, a critical step for the entry of mature oocytes into the spermatheca for fertilization. Furthermore, fos-1 and jun-1 regulate the spermathecalspecific expression of plc-1, a gene that encodes a phospholipase C (PLC) isozyme that is rate-limiting for inositol triphosphate production and ovulation, and overexpression of PLC-1 rescues the ovulation defect in fos-1(RNAi) worms. Unlike fos-1, regulation of ovulation by jun-1 requires genetic interactions with eri-1 and lin-15B, which are involved in the RNA interference pathway and chromatin remodeling, respectively. At least two isoforms of jun-1 are coexpressed with fos-1b in the spermatheca, and different AP-1 dimers formed between these isoforms have distinct effects on the activation of a reporter gene. These findings uncover a novel role for FOS-1 and JUN-1 in the reproductive system and establish C. elegans as a model for studying AP-1 dimerization.

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An essential function of AP-1 heterodimers in Drosophila development

Cited by 23 publications

References 22 publications

Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggyas a Regulator of AP-1-Dependent Developmental Plasticity

Overexpression Screen in Drosophila Identifies Neuronal Roles of GSK-3β/shaggyas a Regulator of AP-1-Dependent Developmental Plasticity

The Stress-response protein prostate-associated gene 4, interacts with c-Jun and potentiates its transactivation

Caenorhabditis elegans FOS-1 and JUN-1 Regulateplc-1Expression in the Spermatheca to Control Ovulation

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