The Effects of Starvation or of Treatment With Cytotoxic Agents on Pregnancy in Mice

Gebhardt, D. O. E.

doi:10.1530/jrf.0.0190519

Cited by 13 publications

(2 citation statements)

References 9 publications

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“…Specifically, knockout of the major mTORC1 components, mTOR or RAPTOR, in mice caused early embryonic lethality shortly after implantation, when embryos must utilize environmental nutrients for development (Guertin et al, 2006). Such a phenotype mimics the temporary fasting-induced embryonic lethality (Gebhardt, 1969). Studies in invertebrate organisms, such as Drosophila melanogaster or C. elegans, also showed that deficiency of mTOR or RAPTOR orthologs caused the developmental arrest and led to death at the postembryonic stage, which phenotypically mimicked the complete or AA-starvation-induced development lethality (Jia et al, 2004;Long et al, 2002;Oldham et al, 2000;Qi et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

A sphingolipid-mTORC1 nutrient-sensing pathway regulates animal development by an intestinal peroxisome relocation-based gut-brain crosstalk

Hua

Chen

et al. 2022

Cell Reports

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Section: Introductionmentioning

confidence: 99%

A sphingolipid-mTORC1 nutrient-sensing pathway regulates animal development by an intestinal peroxisome relocation-based gut-brain crosstalk

Hua

Chen

et al. 2022

Cell Reports

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“…Specifically, knockout of the major mTORC1 components, mTOR or RAPTOR, in mice caused early embryonic lethality shortly after implantation, when embryos must utilize environmental nutrients for development (Guertin et al, 2006). Such a phenotype mimics the temporary fasting-induced embryonic lethality (Gebhardt, 1969). Studies in invertebrate organisms such as Drosophila melanogaster or C. elegans also showed that deficiency of mTOR or RAPTOR orthologs caused developmental arrest and led to death at the postembryonic stage, which phenotypically mimicked the complete or AA starvation-induced development lethality(Jia et al, 2004; Long et al, 2002; Oldham et al, 2000; Qi et al, 2017).…”

Section: Introductionmentioning

confidence: 97%

A lipid-mTORC1 nutrient sensing pathway regulates animal development by peroxisome-derived hormones

Bai

Chen

et al. 2021

Preprint

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Animals have developed many signaling mechanisms that alter cellular and developmental programs in response to changes in nutrients and their derived metabolites, many of which remain to be understood. We recently uncovered that glucosylceramides, a core sphingolipid, act as a critical nutrient signal for overall amino-acid level to promote development by activating the intestinal mTORC1 pathway. However, how the intestinal GlcCer-mTORC1 activity regulates development throughout the whole body is unknown. Through a large-scale genetic screen, we found that the peroxisomes are critical for antagonizing the GlcCer-mTORC1-mediated nutrient signal. Mechanistically, deficiency of glucosylceramide, inactivation of the downstream mTORC1 activity, or prolonged starvation relocated peroxisomes closer to the intestinal apical region to release peroxisomal-beta-oxidation derived hormones that targeting chemosensory neurons to arrest the animal development. Our data illustrated a new gut-brain axis for orchestrating nutrient-sensing dependent development in Caenorhabditis elegans, which may also explain why glucosylceramide and peroxisome become essential in metazoans.

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The embryolethality and localization of antikidney serum in the pregnant mouse, Mus musculus

Gebhardt¹,

Faille-kuyper

Nagel³

1970

Teratology

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The period in which antimouse kidney serum (AKS) was embryolethal in the mouse extended from days 4-15 of pregnancy. The highest sensitivity toward AKS existed at days 10-14.When AKS was localized in the uterus by immunofluorescence the following results were obtained. On day 10 Reichert's membrane, parietal yolk-sac cells, and endodermal cells of the visceral yolk sac, but not the embryo, showed intense fluorescence. By day 12 Reichert's membrane and the parietal yolk-sac cells had lost most of their immunofluorescence. The visceral yolk-sac cells adjacent to the chorioallantoic placenta still stained strongly on day 18 of pregnancy.AKS from which the antiplacental factor(s) were removed retained its embryolethality when injected on day 10. It was localized solely i n the visceral yolk sac.Therefore AKS probably caused embryonic death by damaging the yolk-sac cells.Only during the last days of pregnancy was there any transfer of AKS to the embryos. of staining may then be caused by a reduced structural integrity. Anderson, J. W. 1959 The placental barrier toNo exact explanation C a n be given at gamma-globulin in the rat. Am. J. Anat., 104: present for the lack of immunofluorescence 403430. LITERATURE CITED~~ if uteri from mice injected with normal Baart de la Faille-Kuyper, E. H. 1969 Lupus rabbit Serum (NRS). However, it is likely erythematosus. A clinical and immunohistochemical study of 485 patients. M.D. thesis. that the visceral endodermal cells retain Schotanus and Jens, Utrecht.

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The Effects of Starvation or of Treatment With Cytotoxic Agents on Pregnancy in Mice

Cited by 13 publications

References 9 publications

A sphingolipid-mTORC1 nutrient-sensing pathway regulates animal development by an intestinal peroxisome relocation-based gut-brain crosstalk

A sphingolipid-mTORC1 nutrient-sensing pathway regulates animal development by an intestinal peroxisome relocation-based gut-brain crosstalk

A lipid-mTORC1 nutrient sensing pathway regulates animal development by peroxisome-derived hormones

The embryolethality and localization of antikidney serum in the pregnant mouse, Mus musculus

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