Minutes: Mutants of Drosophila autonomously affecting cell division rate

Morata, Ginés; Ripóll, Pedro

doi:10.1016/0012-1606(75)90330-9

Cited by 906 publications

(676 citation statements)

References 11 publications

Supporting

Mentioning

654

Contrasting

Unclassified

Order By: Relevance

“…49 A similar mechanism was proposed to account for the delayed larval development and reduced body size of Drosophila minute mutants harboring hypomorphic mutations in ribosomal proteins. 50 When surrounded by wild-type cells, minute clones are outcompeted and disappear (for review, see Amoyel and Bach 51 ). Thus, such cell competition phenomena might also contribute to the replacement of Nle-deficient crypt cells by cells that have escaped recombination.…”

Section: Discussionmentioning

confidence: 99%

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

et al. 2015

View full text Add to dashboard Cite

International audienceRibosome biogenesis is an essential cellular process. Its impairment is associated with developmental defects and increased risk of cancer. The in vivo cellular responses to defective ribosome biogenesis and the underlying molecular mechanisms are still incompletely understood. In particular, the consequences of impaired ribosome biogenesis within the intestinal epithelium in mammals have not been investigated so far. Here we adopted a genetic approach to investigate the role of Notchless (NLE), an essential actor of ribosome biogenesis, in the adult mouse intestinal lineage. Nle deficiency led to defects in the synthesis of large ribosomal subunit in crypts cells and resulted in the rapid elimination of intestinal stem cells and progenitors through distinct types of cellular responses, including apoptosis, cell cycle arrest and biased differentiation toward the goblet cell lineage. Similar observations were made using the rRNA transcription inhibitor CX-5461 on intestinal organoids culture. Importantly, we found that p53 activation was responsible for most of the cellular responses observed, including differentiation toward the goblet cell lineage. Moreover, we identify the goblet cell-specific marker Muc2 as a direct transcriptional target of p53. Nle-deficient ISCs and progenitors disappearance persisted in the absence of p53, underlying the existence of p53-independent cellular responses following defective ribosome biogenesis. Our data indicate that NLE is a crucial factor for intestinal homeostasis and provide new insights into how perturbations of ribosome biogenesis impact on cell fate decisions within the intestinal epithelium

show abstract

Section: Discussionmentioning

confidence: 99%

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

et al. 2015

View full text Add to dashboard Cite

show abstract

“…2D). When we increased the size of the eld clones further by using a Minute mutation to slow the growth of the surrounding wild-type tissue (Morata and Ripoll 1975), a complete block of differentiation within the clone was observed frequently, although this usually did not encompass the entire clone (Fig. 2E,F).…”

Section: Eyelid Affects Patterning Of the Eye Imaginal Discmentioning

confidence: 99%

eyelidantagonizes wingless signaling during Drosophiladevelopment and has homology to the Bright family of DNA-binding proteins

Treisman

Luk²,

Rubin³

et al. 1997

Genes Dev.

115

View full text Add to dashboard Cite

In Drosophila, pattern formation at multiple stages of embryonic and imaginal development depends on the same intercellular signaling pathways. We have identified a novel gene, eyelid (eld), which is required for embryonic segmentation, development of the notum and wing margin, and photoreceptor differentiation. In these tissues, eld mutations have effects opposite to those caused by wingless (wg) mutations. eld encodes a widely expressed nuclear protein with a region homologous to a novel family of DNA-binding domains. Based on this homology and on the phenotypic analysis, we suggest that Eld could act as a transcription factor antagonistic to the Wg pathway.

show abstract

“…But we know that in a mosaic animal, clones of cells heterozygous for a deficiency grow more slowly than normal cells or cells with a duplication; in extreme cases, cells carrying a deficiency may not be viable or may disappear due to cell competition, a process which can eliminate clones in all body regions except in the abdomen (Morata and Ripoll, 1975;Ripoll, 1980;Simpson, 1981;Simpson and Morata, 1981). We therefore expect that our aneuploid cells will grow better when their X chromosomes are transcribed at a high rate than when they are transcribed at a low rate.…”

Section: Discussionmentioning

confidence: 99%

A small region on the X chromosome of Drosophila regulates a key gene that controls sex determination and dosage compensation

Steinmann‐Zwicky

Nöthiger

1985

Cell

View full text Add to dashboard Cite

A small region on the X chromosome of Drosophila regulates a key gene that controls sex determination and dosage compensation A small region on the X chromosome of Drosophila regulates a key gene that controls sex determination and dosage compensation AbstractIn Drosophila, flies with two X chromosomes are females, with one X chromosome, males. We investigated the presence of sex determining factors on the X chromosome by constructing genotypes with one X and various X-chromosomal duplications. We found that female determining factors are not evenly distributed along the X chromosome as had been previously postulated. A distal duplication covering 35% of the X chromosome promotes female differentiation, a much larger proximal duplication of 60% results in male differentiation. The strong feminizing effect of distal duplications originates from a small segment that, when present in two doses, activates Sxl, a key gene for sex determination and dosage compensation. Our results suggest that Sxl can be activated to intermediate levels. In Drosophila, flies with two X chromosomes are females, with one X chromosome, males. We investigated the presence of sex determining factors on the X chromosome by constructing genotypes with one X and various X-chromosomal duplications.We found that female determining factors are not evenly distributed along the X chromosome as had been previously postulated.A distal duplication covering 35% of the X chromosome promotes female differentiation, a much larger proximal duplication of 60% results in male differentiation.The strong feminizing effect of distal duplications originates from a small segment that, when present in two doses, activates Sxl, a key gene for sex determination and dosage compensation. Our results suggest that Sxl can be activated to intermediate levels.

show abstract

Minutes: Mutants of Drosophila autonomously affecting cell division rate

Cited by 906 publications

References 11 publications

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

Ribosome biogenesis dysfunction leads to p53-mediated apoptosis and goblet cell differentiation of mouse intestinal stem/progenitor cells

eyelidantagonizes wingless signaling during Drosophiladevelopment and has homology to the Bright family of DNA-binding proteins

A small region on the X chromosome of Drosophila regulates a key gene that controls sex determination and dosage compensation

Contact Info

Product

Resources

About