Skip to main content

A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans

Wang, Hongyuan, Zhao, Yuan, Ezcurra, Marina, Benedetto, Alexandre, Gilliat, Ann F., Hellberg, Josephine, Ren, Ziyu, Galimov, Evgeniy R., Athigapanich, Trin, Girstmair, Johannes, and others. (2018) A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans. npj Aging and Mechanisms of Disease, 4 (1). ISSN 2056-3973. (doi:10.1038/s41514-018-0025-3) (KAR id:74209)

PDF Publisher pdf
Language: English

Creative Commons Licence
This work is licensed under a Creative Commons Attribution 4.0 International License.
Download (2MB) Preview
PDF Author's Accepted Manuscript
Language: English

Restricted to Repository staff only
Contact us about this Publication
Official URL


A long-standing belief is that aging (senescence) is the result of stochastic damage accumulation. Alternatively, senescent pathology may also result from late-life, wild-type gene action (i.e., antagonistic pleiotropy, as argued by Williams) leading to non-adaptive run-on of developmental programs (or quasi-programs) (as suggested more recently by Blagosklonny). In this study, we use existing and new data to show how uterine tumors, a prominent form of senescent pathology in the nematode Caenorhabditis elegans, likely result from quasi-programs. Such tumors develop from unfertilized oocytes which enter the uterus and become hypertrophic and replete with endoreduplicated chromatin masses. Tumor formation begins with ovulation of unfertilized oocytes immediately after exhaustion of sperm stocks. We show that the timing of this transition between program and quasi-program (i.e., the onset of senescence), and the onset of tumor formation, depends upon the timing of sperm depletion. We identify homology between uterine tumors and mammalian ovarian teratomas, which both develop from oocytes that fail to mature after meiosis I. In teratomas, futile activation of developmental programs leads to the formation of differentiated structures within the tumor. We report that older uterine tumors express markers of later embryogenesis, consistent with teratoma-like activation of developmental programs. We also present evidence of coupling of distal gonad atrophy to oocyte hypertrophy. This study shows how the Williams Blagosklonny model can provide a mechanistic explanation of this component of C. elegans aging. It also suggests etiological similarity between teratoma and some forms of senescent pathology, insofar as both are caused by quasi-programs.

Item Type: Article
DOI/Identification number: 10.1038/s41514-018-0025-3
Divisions: Faculties > Sciences > School of Biosciences
Depositing User: Marina Ezcurra
Date Deposited: 31 May 2019 15:28 UTC
Last Modified: 22 Jan 2020 04:12 UTC
Resource URI: (The current URI for this page, for reference purposes)
Ezcurra, Marina:
  • Depositors only (login required):


Downloads per month over past year