A Phg2-Adrm1 Pathway Participates in the Nutrient-controlled Developmental Response in<i>Dictyostelium</i>

Cherix, Nathalie; Froquet, Romain Bruno; Charette, Steve J.; Blanc, Cédric; Letourneur, François; Cosson, Pierre

doi:10.1091/mbc.e06-07-0619

Cited by 17 publications

(21 citation statements)

References 26 publications

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“…Phosphoproteome analysis suggested that polyphosphate may have caused Adrm1 phosphorylation at residue T280 in three of the four trials, although polyphosphate did not significantly affect levels of Adrm1 (Table S1). To determine whether cells lacking Adrm1 have altered proteasome activity, we examined the proteasome activity levels of wild-type and adrm1 − cells (Cherix et al, 2006). Compared to wild-type cells, adrm1 − cells had abnormally low levels of proteasome activity ( Fig.…”

Section: Polyphosphate Induces Development In the Presence Of Nutrientsmentioning

confidence: 99%

“…2A). Unlike wild-type cells, Dictyostelium cells lacking Adrm1 transition from vegetative growth to development while still in the presence of nutrients, suggesting a defect in the pre-starvation response and/or the GDT (Cherix et al, 2006). To determine whether the starvation-induced GDT is associated with a decrease in proteasome activity, the proteasome activity levels of starved cells was measured.…”

Section: Polyphosphate Induces Development In the Presence Of Nutrientsmentioning

confidence: 99%

“…Unlike wild-type cells, adrm1 − cells express early onset development genes and begin to aggregate while in the presence of nutrients (Cherix et al, 2006). To determine whether high levels of extracellular polyphosphate might have effects similar to the loss of Adrm1, we cultured cells with polyphosphate in HL5, a nutrientrich medium, for 24 h. Using spectrophotometry to measure total protein, we had previously observed that polyphosphate increases protein per cell by 1.57±0.06 fold (Suess and Gomer, 2016), and by scanning Coomassie-stained gels (Fig.…”

Section: Polyphosphate Induces Development In the Presence Of Nutrientsmentioning

confidence: 99%

“…S2B). Cells lacking Adrm1 phenocopy many of the effects initiated by extracellular polyphosphate including expression of CsA and formation of aggregates in the presence of nutrients (Cherix et al, 2006), as well as decreased vegetative proteasome activity. Whether or not polyphosphate affects Adrm1 in addition to decreasing other proteasome subunits to inhibit proteasome activity warrants further investigation.…”

Section: Proteasome Inhibition Alone Is Not Sufficient To Induce Devementioning

confidence: 99%

“…The cells used were Dictyostelium wild-type Ax2, pakD − (DBS0350281) (Garcia et al, 2014), erk1 − (DBS0350622) (Gaskins et al, 1994), pkbA − (DBS0349876) (Meili et al, 1999), pkbA − /pkgB − (DBS0236785) (Meili et al, 2000), rasC − (DBS0236853) (Daniel et al, 1994), napA − (DBS0236596) (Ibarra et al, 2006), adrm1 − (DBS0238203) (Cherix et al, 2006), fslB − (DBS0350230) (Prabhu and Eichinger, 2006), fslK − (DBS0350229) (Prabhu and Eichinger, 2006), ctnA − (DBS0235624) (Brock and Gomer, 1999), i6kA − (DBS0236426) (Luo et al, 2003), grlB − (DBS0350074) (Prabhu and Eichinger, 2006), grlE − (DBS0350075) (Prabhu and Eichinger, 2006), grlH − (DBS0350226) (Prabhu and Eichinger, 2006), cfaD − (DBS0302444) (Bakthavatsalam et al, 2008), lst8 − (DBS0236517) (Lee et al, 2005), ppk1 − (DBS0350685) (Livermore et al, 2016) and cnrN − (DBS0302655) (Tang and Gomer, 2008). Mutant genotypes were verified by PCR, and cells were kept under constant selection.…”

Section: Dictyostelium and Human Leukemia Cell Culturementioning

confidence: 99%

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Extracellular polyphosphate signals through Ras and Akt to prime Dictyostelium discoideum cells for development

Suess

Watson

Chen

et al. 2017

Journal of Cell Science

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Linear chains of five to hundreds of phosphates called polyphosphate are found in organisms ranging from bacteria to humans, but their function is poorly understood. In Dictyostelium discoideum, polyphosphate is used as a secreted signal that inhibits cytokinesis in an autocrine negative feedback loop. To elucidate how cells respond to this unusual signal, we undertook a proteomic analysis of cells treated with physiological levels of polyphosphate and observed that polyphosphate causes cells to decrease levels of actin cytoskeleton proteins, possibly explaining how polyphosphate inhibits cytokinesis. Polyphosphate also causes proteasome protein levels to decrease, and in both Dictyostelium and human leukemia cells, decreases proteasome activity and cell proliferation. Polyphosphate also induces Dictyostelium cells to begin development by increasing expression of the cell-cell adhesion molecule CsA (also known as CsaA) and causing aggregation, and this effect, as well as the inhibition of proteasome activity, is mediated by Ras and Akt proteins. Surprisingly, Ras and Akt do not affect the ability of polyphosphate to inhibit proliferation, suggesting that a branching pathway mediates the effects of polyphosphate, with one branch affecting proliferation, and the other branch affecting development.

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Section: Polyphosphate Induces Development In the Presence Of Nutrientsmentioning

confidence: 99%

Section: Polyphosphate Induces Development In the Presence Of Nutrientsmentioning

confidence: 99%

Section: Polyphosphate Induces Development In the Presence Of Nutrientsmentioning

confidence: 99%

Section: Proteasome Inhibition Alone Is Not Sufficient To Induce Devementioning

confidence: 99%

Section: Dictyostelium and Human Leukemia Cell Culturementioning

confidence: 99%

See 3 more Smart Citations

Extracellular polyphosphate signals through Ras and Akt to prime Dictyostelium discoideum cells for development

Suess

Watson

Chen

et al. 2017

Journal of Cell Science

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Comprehensive analysis of 20q13 genes in ovarian cancer identifies ADRM1 as amplification target

Fejzo

Dering

Ginther

et al. 2008

Genes Chromosomes & Cancer

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Approximately 25,000 ovarian cancers are diagnosed in the US annually, and 75% of cases are in the advanced stage when they are largely incurable. There is a critical need for improved early detection tools and development of novel treatments. Because chromosome band 20q13 is a commonly DNA amplified region in ovarian cancer and increase in 20q13 copy number may be an early event, we examined the DNA amplification and RNA expression pattern of 239 microarray probes mapping to this region with the goal of identifying gene(s) associated with ovarian cancer. Using Agilent expression microarray analysis and FISH to tumor tissue arrays, we narrowed the candidates to 19 genes that were consistently overexpressed in a subset of tumors amplified for both ZNF217 and TPD54, although, interestingly the candidates do not include these two amplified genes. Unsupervised clustering of 225 ovarian samples with respect to RNA expression of these 19 genes allowed identification of a 20q-amplified subset of 51 (23%) tumors and this subset was significantly correlated with poor outcome. Of the 19 candidate genes in this subset, ADRM1 overexpression was the most highly correlated with amplification, was amplified in a higher percentage of tumors than ZNF217 and TPD54, and was significantly upregulated with respect to stage, recurrence and metastasis. In addition, overexpression of ADRM1 correlates significantly with shorter time to recurrence and overall survival. Functional analysis is now warranted to determine whether ADRM1 is a target for early screening and/or therapy for ovarian cancer.

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Knockdown of ovarian cancer amplification target ADRM1 leads to downregulation of GIPC1 and upregulation of RECK

Fejzo¹,

Ginther²,

Dering³

et al. 2011

Genes Chromosomes & Cancer

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Approximately 25,000 ovarian cancers are diagnosed in the United States annually, and 75% of cases are in the advanced stage when they are largely incurable. There is a critical need for improved early detection tools and development of novel treatments. Recently, we showed that among 20q13-amplified genes in ovarian cancer, ADRM1 overexpression was the most highly correlated with amplification and was significantly upregulated with respect to stage, recurrence, and metastasis. In addition, overexpression of ADRM1 correlated significantly with shorter time to recurrence and overall survival. Herein, array-CGH and microarray expression of ovarian cancer cell lines provides evidence consistent with the primary tumor data that ADRM1 is a 20q13 amplification target. Knockdown of ADRM1 in amplified ovarian cell-line OAW42 results in downregulation of growth factor GIPC1 and upregulation of tumor-suppressor RECK RNA and protein. In our dataset of 141 ovarian primary tumors, ADRM1 overexpression significantly correlates with GIPC1 overexpression. In addition, there is a significant anticorrelation between ADRM1 overexpression and RECK expression. Further research is necessary to determine whether targeting knockdown of ADRM1 in 20q13-amplified ovarian cancers results in growth inhibition and tumor suppression via downstream targets GIPC1 and RECK.

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A Phg2-Adrm1 Pathway Participates in the Nutrient-controlled Developmental Response inDictyostelium

Cited by 17 publications

References 26 publications

Extracellular polyphosphate signals through Ras and Akt to prime Dictyostelium discoideum cells for development

Extracellular polyphosphate signals through Ras and Akt to prime Dictyostelium discoideum cells for development

Comprehensive analysis of 20q13 genes in ovarian cancer identifies ADRM1 as amplification target

Knockdown of ovarian cancer amplification target ADRM1 leads to downregulation of GIPC1 and upregulation of RECK

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