Dpp signaling and the induction of neoplastic tumors by caspase-inhibited apoptotic cells in
 Drosophila

Pérez-Garijo, Ainhoa; Martín, Francisco A.; Struhl, Gary; Morata, Ginés

doi:10.1073/pnas.0508966102

Cited by 68 publications

(43 citation statements)

References 35 publications

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“…35) In such a context, p35 expression-mediated inhibition of apoptosis allows some cells to survive as undead cells, and they secrete signals to promote further the proliferation of surrounding cells. [36][37][38][39] Therefore, even in the context of CG17836/Xrp1 overexpression, co-expression of p35 might also positively affect antennal duplication via enhancement of surrounding cell proliferation and/or secreted signaling molecules induced by the undead cells.…”

Section: Possible Mechanisms Of Ectopic Antennal Formation By Cg17836mentioning

confidence: 99%

Ectopic Antenna Induction by Overexpression of CG17836/Xrp1 Encoding an AT-Hook DNA Binding Motif Protein in Drosophila

Tsurui-Nishimura

Nguyen

Katsuyama

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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Section: Possible Mechanisms Of Ectopic Antennal Formation By Cg17836mentioning

confidence: 99%

Ectopic Antenna Induction by Overexpression of CG17836/Xrp1 Encoding an AT-Hook DNA Binding Motif Protein in Drosophila

Tsurui-Nishimura

Nguyen

Katsuyama

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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“…In certain circumstances, however, the acquisition by the latter of some additional property may turn tumour cells into super-competitors, thus reversing the situation. It has been argued that cell competition may be a major factor in tumour progression in circumstances in which tumour cells are able to outcompete normal cells (Moreno and Basler, 2004;Perez-Garijo et al, 2005;Moreno, 2007).…”

Section: Research Articlementioning

confidence: 99%

“…Obviously, the elimination of weaker or slow-dividing cells within an imaginal disc may contribute to the general fitness of the disc. The ability of fast-dividing cells to eliminate slow ones has suggested that cell competition may be a relevant factor in the colonisation of tissues by tumorous cells (Perez-Garijo et al, 2005;Moreno and Basler, 2004;Moreno, 2007).…”

Section: Introductionmentioning

confidence: 99%

Cell competition, growth and size control in theDrosophilawing imaginal disc

2009

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We report here experiments aimed at understanding the connections between cell competition and growth in the Drosophila wing disc. The principal assay has been to generate discs containing marked cells that proliferate at different rates and to study their interactions and their contribution to the final structure. It is known that single clones of fast-dividing cells within a compartment may occupy the larger part of the compartment without affecting its size. This has suggested the existence of interactions involving cell competition between fast-and slow-dividing cells directed to accommodate the contribution of each cell to the final compartment. Here we show that indeed fast-dividing cells can outcompete slow-dividing ones in their proximity. However, we argue that this elimination is of little consequence because preventing apoptosis, and therefore cell competition, in those compartments does not affect the size of the clones or the size of the compartments. Our experiments indicate that cells within a compartment proliferate autonomously at their own rate. The contribution of each cell to the compartment is exclusively determined by its division rate within the frame of a size control mechanism that stops growth once the compartment has reached the final arresting size. This is supported by a computer simulation of the contribution of individual fast clones growing within a population of slower dividing cells and without interacting with them. The values predicted by the simulation are very close to those obtained experimentally.

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“…Similarly, the neoplastic tumors induced by wingless mutant cells blocked for apoptosis (Perez-Garijo et al 2005) also appear to be due to the loss of lgl from the wingless mutant chromosome studied (G. Morata, personal communication). We even found that the numb[1] stock (available at the Bloomington Stock Center), which disrupts the prototypical asymmetric cell fate determinant in Drosophila (Uemura et al 1989;Rhyu et al 1994), is deficient for lgl.…”

Section: Discussionmentioning

confidence: 99%

Frequent Unanticipated Alleles of lethal giant larvae in Drosophila Second Chromosome Stocks

et al. 2009

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Forty years ago, a high frequency of lethal giant larvae (lgl) alleles in wild populations of Drosophila melanogaster was reported. This locus has been intensively studied for its roles in epithelial polarity, asymmetric neural divisions, and restriction of tissue proliferation. Here, we identify a high frequency of lgl alleles in the Bloomington second chromosome deficiency kit and the University of California at Los Angeles Bruinfly FRT40A-lethal P collection. These unrecognized aberrations confound the use of these workhorse collections for phenotypic screening or genetic mapping. In addition, we determined that independent alleles of insensitive, reported to affect asymmetric cell divisions during sensory organ development, carry lgl deletions that are responsible for the observed phenotypes. Taken together, these results encourage the routine testing of second chromosome stocks for second-site alleles of lgl.

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Dpp signaling and the induction of neoplastic tumors by caspase-inhibited apoptotic cells in Drosophila

Abstract: In Drosophila, stresses such as x-irradiation or severe heat shock can cause most epidermal cells to die by apoptosis. Yet, the remaining cells recover from such assaults and form normal adult structures, indicating that they undergo extra growth to replace the lost cells.

Cited by 68 publications

References 35 publications

Ectopic Antenna Induction by Overexpression of <i>CG17836/Xrp1</i> Encoding an AT-Hook DNA Binding Motif Protein in <i>Drosophila</i>

Ectopic Antenna Induction by Overexpression of <i>CG17836/Xrp1</i> Encoding an AT-Hook DNA Binding Motif Protein in <i>Drosophila</i>

Cell competition, growth and size control in theDrosophilawing imaginal disc

Frequent Unanticipated Alleles of lethal giant larvae in Drosophila Second Chromosome Stocks

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