Fig. 1.

Theories of aging and uterine tumor development. a, b Alternative models for how wild-type genes cause senescence (pathogenic action of alleles exhibiting antagonistic pleiotropy). a Disposable soma model. Wild-type genes promote reproduction at the expense of somatic maintenance processes that prevent the damage that causes aging. b Williams Blagosklonny model. Continued action of wild-type genes in later life leads to run-on of developmental programs (quasi-programs) causing development of senescent pathology. c, d Senescent uterine tumors in C. elegans hermaphrodites. c Stages of development of uterine tumors. Dotted lines delineate uterine contents. Scale bar, 50 μm. d Schematic representation of uterine tumor development, consistent with Williams Blagosklonny model. As argued in this study, the point of origin of pathophysiology is immediately after fertilization with the last sperm in the spermatheca; this is the point of transition from program to quasi-program. Red, promoting senescent pathology