Aging is a phenomenon that brings about the onset of many diseases and increases mortality. Understanding aging mechanisms can help us increase longevity and delay the onset of multiple chronic diseases. It has been previously observed that dietary restriction is a method that increases lifespan and delays the loss of function caused by age-associated pathologies. We used the roundworm, Caenhorbabditis elegans, to dissect the mechanisms of dietary restriction-induced longevity. Specifically, we focused on the phenomenon of adult reproductive diapause (ARD). ARD is induced when pre-reproductive juvenile larvae are subjected to starvation. Upon reintroduction to food after prolonged starvation, ARD worms undergo a morphological rejuvenation and resume a normal lifespan. Mechanisms that control post-diapause recovery are still quite unknown. We have found that the TGF-β/BMP signaling pathway is required for post ARD rejuvenation. The TGF-beta signaling pathway is a critical factor for growth processes including cell growth, differentiation, embryonic development, and much more. We aimed to characterize the role of this signaling pathway in ARD maintenance and post-ARD recovery. We hypothesized that TGF-β/BMP mutants accumulate excessive amounts of cellular damage during ARD and are unable to recover from ARD. To address this hypothesis, we analyzed markers of cellular aging among diapaused animals using fluorescent microscopy, in both wild type and TGF-β/BMP mutants. Using transgenic fluorescent reporter strains we examined pH, nucleolar morphology, mitochondria, and cytoskeleton and nucleoskeleton integrity for aging-associated phenotypes. These insights can help us understand the role of the conserved TGF-β/BMP pathway in dietary restriction induced longevity.