Wingless signaling regulates winner/loser status in <i>Minute</i> cell competition

Akai, Nanami; Igaki, Tatsushi; Ohsawa, Seiji

doi:10.1111/gtc.12568

Cited by 11 publications

(8 citation statements)

References 24 publications

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“…Despite hypotheses that Rp +/- cells might be less efficient at capturing Dpp [25], or experience elevated Wg signaling [26], representative target genes for Dpp and Wg signals were not affected in RpS3 +/- and RpS17 +/- wing discs. There were also no gene expression changes of signature genes for Ras, Hh, or Salvador-Warts-Hippo signaling (S2 Table).…”

Section: Resultsmentioning

confidence: 99%

Drosophila RpS12 controls translation, growth, and cell competition through Xrp1

Kiparaki

Folgado

et al. 2019

PLoS Genet

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Whereas complete loss of Rp function is generally lethal, most heterozygous Rp mutants grow more slowly and are subject to competitive loss from mosaics tissues that also contain wild type cells. The rpS12 gene has a special role in the cell competition of other Ribosomal Protein (Rp) mutant cells in Drosophila. Elimination by cell competition is promoted by higher RpS12 levels and prevented by a specific rpS12 mis-sense mutation, identifying RpS12 as a key effector of cell competition due to mutations in other Rp genes. Here we show that RpS12 is also required for other aspects of Rp mutant phenotypes, including hundreds of gene expression changes that occur in ‘Minute’ Rp heterozygous wing imaginal discs, overall translation rate, and the overall rate of organismal development, all through the bZip protein Xrp1 that is one of the RpS12-regulated genes. Our findings outline the regulatory response to mutations affecting essential Rp genes that controls overall translation, growth, and cell competition, and which may contribute to cancer and other diseases.

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Section: Resultsmentioning

confidence: 99%

Drosophila RpS12 controls translation, growth, and cell competition through Xrp1

Kiparaki

Folgado

et al. 2019

PLoS Genet

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“…The following strains were used: dilp8 ex (Pierre Leopold), 10xSTAT-GFP (Erika A. Bach), UAS-CD8-PARP-Venus (Yash Hiromi), UAS-S/G2/M-Green (Kaoru Sugimura), hh-gal4 (Tetsuya Tabata), UAS-Dronc DN (Sharad Kumar), wg-gal4 (Jean-Paul Vincent), scrib 1 [64], UAS-Puc [65], UAS-RpS3 [66], RpS3 Plac92 , RpL19 K03704 , RpS17 4 , dsh 3 , nmo P1 (nmo-lacZ), nkd 04869a (nkd-lacZ), wg 17en40cP1 (wg-lacZ), msn 06946 (msn-lacZ), dilp8 MI00727 (eGFP trap), UAS-p35, UAS-Wg, UAS-dsh-RNAi, Df(3L)H99, nub-gal4, en-gal4, wg , TRE-DsRed, act-gal4 (Bloomington Stock Center), UAS-Arm S10 , ecd 1 , wg l-8 , FRT82B, GMR-hid, CL3R (the Drosophila Genomics and Genetic Resources, DGGR), UAS-tcf-RNAi, UAS-dsh-RNAi (National Institute of Genetics Stock Center), and UAS-dilp8-RNAi (Vienna Drosophila RNAi Center, VDRC).…”

Section: Fly Strainsmentioning

confidence: 99%

Epithelial cell-turnover ensures robust coordination of tissue growth in Drosophila ribosomal protein mutants

et al. 2021

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Highly reproducible tissue development is achieved by robust, time-dependent coordination of cell proliferation and cell death. To study the mechanisms underlying robust tissue growth, we analyzed the developmental process of wing imaginal discs in Drosophila Minute mutants, a series of heterozygous mutants for a ribosomal protein gene. Minute animals show significant developmental delay during the larval period but develop into essentially normal flies, suggesting there exists a mechanism ensuring robust tissue growth during abnormally prolonged developmental time. Surprisingly, we found that both cell death and compensatory cell proliferation were dramatically increased in developing wing pouches of Minute animals. Blocking the cell-turnover by inhibiting cell death resulted in morphological defects, indicating the essential role of cell-turnover in Minute wing morphogenesis. Our analyses showed that Minute wing discs elevate Wg expression and JNK-mediated Dilp8 expression that causes developmental delay, both of which are necessary for the induction of cell-turnover. Furthermore, forced increase in Wg expression together with developmental delay caused by ecdysone depletion induced cell-turnover in the wing pouches of non-Minute animals. Our findings suggest a novel paradigm for robust coordination of tissue growth by cell-turnover, which is induced when developmental time axis is distorted.

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“…Supercompetition by Hippo pathway mutant cells was also observed in cultured mammalian fibroblast cells (Mamada, Sato, Ota, & Sasaki, 2015). Importantly, Minute cell competition (Akai, Igaki, & Ohsawa, 2018). Cells with higher JAK-STAT signaling were also found to be supercompetitors that eliminate neighboring wild-type cells in a hid-dependent manner (Rodrigues et al, 2012).…”

Section: Other Types Of Cell Competition That Select Fitter Cellsmentioning

confidence: 83%

“…In flies, Wingless (Wg) signaling was also shown to determine the loser/winner status of cells, as cells with higher Wg signaling activity cause elimination of neighboring cells with lower Wg signaling activity (Vincent et al., ). Interestingly, activation of Wg signaling in M /+ losers or downregulation of Wg signaling in wild‐type winners suppresses Minute cell competition (Akai, Igaki, & Ohsawa, ). Cells with higher JAK‐STAT signaling were also found to be supercompetitors that eliminate neighboring wild‐type cells in a hid ‐dependent manner (Rodrigues et al., ).…”

Section: Selection Of Fitter Cells: Minute or Myc‐induced Cell Competmentioning

confidence: 99%

Cell competition: Emerging mechanisms to eliminate neighbors

Nagata

Igaki

2018

Dev Growth Differ

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Cell competition is a context‐dependent cell elimination through short‐range cell–cell interaction, in which cells with higher fitness eliminate neighboring less‐fit or oncogenic cells within the growing tissue. Cell competition can be triggered by many different factors such as heterozygous mutations in the ribosomal protein genes (which are called “Minute” mutations), elevated Myc, Yorkie/YAP, Wg/Wnt, JAK‐STAT, Ras, or Src activity, and loss of Mahjong/VprBP, endocytic pathway components, or apicobasal cell polarity. Studies on the mechanisms and roles of cell competition have suggested that cell competition can be divided into two types: selection of fitter cells or elimination of oncogenic cells. The former type of cell competition includes Minute or Myc‐induced cell competition that is considered to be dependent on the relative level of protein synthesis. The later type of cell competition includes tumor‐suppressive cell competition triggered by loss of cell polarity genes such as scribble (scrib) or discs large (dlg). Genetic studies in Drosophila during the past decade have provided significant progress in understanding the mechanisms of these phenomena. At the same time, these studies have now raised new questions; how do different mechanisms contribute or cooperate to drive cell competition, do common mechanisms exist in different types of cell competition, and what are the physiological roles of these cell competition phenomena?

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Wingless signaling regulates winner/loser status in Minute cell competition

Cited by 11 publications

References 24 publications

Drosophila RpS12 controls translation, growth, and cell competition through Xrp1

Drosophila RpS12 controls translation, growth, and cell competition through Xrp1

Epithelial cell-turnover ensures robust coordination of tissue growth in Drosophila ribosomal protein mutants

Cell competition: Emerging mechanisms to eliminate neighbors

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