Monsters in the uterus: teratoma-like tumors in senescent C. elegans result from a parthenogenetic quasi-program

Wang, Hongyuan; Zhang, Zhizhou; Gems, David

doi:10.18632/aging.101486

Cited by 18 publications

(18 citation statements)

References 6 publications

(8 reference statements)

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“…In another example, activation of embryogenetic functions in unfertilized oocytes in the uterus leads to extreme polyploidy, cellular hypertrophy and teratoma-like tumors ( Fig. 1A) (McGee et al, 2012;Wang et al, 2018a;Wang et al, 2018b). In both cases, quasi-programs promoted by wild-type gene action contribute to the development of major senescent pathology.…”

Section: Antagonistic Pleiotropy and Programmatic Mechanisms As Consementioning

confidence: 99%

“…Insofar as the term program implies complex function and promotion of fitness , C. elegans intestinal resource reallocation may be referred to as a costly program. By contrast, development of uterine teratomas is the result of a quasi-program (Wang et al, 2018a;Wang et al, 2018b) (Fig. 6A), since a fitness benefit from having tumors is difficult to envisage.…”

Section: Quasi-programs Vs Costly Programs As Ubiquitous Causes Of Sementioning

confidence: 99%

“…Subsequently, declining stem cell division (conceivably adaptive) (Kocsisova et al, 2019) and run-on of PA promotes distal gonad atrophy and fragmentation (de la Guardia et al, 2016). Unfertilized oocytes fail to complete meiosis, enter the uterus and develop into teratoma-like tumors containing massively polyploid chromatin masses (Golden et al, 2007) which appears to result, as in mammalian ovarian teratomas, from embryonic quasi-programs (Wang et al, 2018a;Wang et al, 2018b). B.…”

Section: Referencesmentioning

confidence: 99%

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Semelparity and Reproductive Death in <em>Caenorhabditis elegans</em>

Gems¹,

Kern²,

Nour³

et al. 2020

Preprint

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In some species of salmon, reproductive maturity triggers the development of massive pathology resulting from reproductive effort, leading to rapid post-reproductive death. Such reproductive death, which occurs in many semelparous organisms (with a single bout of reproduction), can be prevented by blocking reproductive maturation, and this can increase lifespan dramatically. Reproductive death is often viewed as distinct from senescence in iteroparous organisms (with multiple bouts of reproduction) such as humans. Here we review the evidence that reproductive death occurs in C. elegans and discuss what this means for its use as a model organism to study aging. Inhibiting insulin/IGF-1 signaling and germline removal suppresses reproductive death and greatly extends lifespan in C. elegans, but can also extend lifespan to a small extent in iteroparous organisms. We argue that mechanisms of senescence operative in reproductive death exist in a less catastrophic form in iteroparous organisms, particularly those involving costly resource reallocation, and exhibiting endocrine-regulated plasticity. Thus, mechanisms of senescence in semelparous organisms (including plants) and iteroparous ones form an etiological continuum. Therefore understanding mechanisms of reproductive death in C. elegans can teach us about some mechanisms of senescence that are operative in iteroparous organisms.

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Section: Antagonistic Pleiotropy and Programmatic Mechanisms As Consementioning

confidence: 99%

Section: Quasi-programs Vs Costly Programs As Ubiquitous Causes Of Sementioning

confidence: 99%

Section: Referencesmentioning

confidence: 99%

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Semelparity and Reproductive Death in <em>Caenorhabditis elegans</em>

Gems¹,

Kern²,

Nour³

et al. 2020

Preprint

Self Cite

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show abstract

“…Rapamycin inhibits growth and slows geroconversion, which is a continuation of growth. In analogous fashion, organismal aging is a continuation of developmental growth [90][91][92][93][94][95][96][97][98]. Rapamycin (at high doses) slows cell proliferation within the organism, causing leucopenia, thrombocytopenia and mucositis and also decelerates organismal aging and its manifestations: age-related diseases [92].…”

Section: Cell Culture and The Organismmentioning

confidence: 99%

Rapamycin, proliferation and geroconversion to senescence

Blagosklonny

2018

Cell Cycle

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Rapamycin inhibits cell proliferation, yet preserves (re)-proliferative potential (RPP). RPP is a potential of quiescent cells that is lost in senescent cells. mTOR drives conversion from quiescence to senescence (geroconversion). By suppressing geroconversion, rapamycin preserves RPP. Geroconversion is characterized by proliferation-like levels of phospho-S6K/S6/4E-BP1 in nonproliferating cells arrested by p16 and/or p21. mTOR-driven geroconversion is associated with cellular hyperfunction, which in turn leads to organismal aging manifested by age-related diseases.

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“…I have explicitly stated as such even in my article titled "Aging is not programmed: genetic pseudo-program a shadow of development growth" (PMID: 24240128). Aging is a normal continuation of the normal developmental program, so it is NOT a program but a purposeless, unintended quasi-program [10–16]. Yet, aging is also a deadly disease because it inevitably leads to death.…”

Section: Endless Debate On Aging and Diseasementioning

confidence: 99%

Disease or not, aging is easily treatable

Blagosklonny

2018

Aging

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Is aging a disease? It does not matter because aging is already treated using a combination of several clinically-available drugs, including rapamycin. Whether aging is a disease depends on arbitrary definitions of both disease and aging. For treatment purposes, aging is a deadly disease (or more generally, pre-disease), despite being a normal continuation of normal organismal growth. It must and, importantly, can be successfully treated, thereby delaying classic age-related diseases such as cancer, cardiovascular and metabolic diseases, and neurodegeneration.

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Monsters in the uterus: teratoma-like tumors in senescent C. elegans result from a parthenogenetic quasi-program

Cited by 18 publications

References 6 publications

Semelparity and Reproductive Death in <em>Caenorhabditis elegans</em>

Semelparity and Reproductive Death in <em>Caenorhabditis elegans</em>

Rapamycin, proliferation and geroconversion to senescence

Disease or not, aging is easily treatable

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