Senescence gives insights into the morphogenetic evolution of anamniotes

Abstract

Senescence represents a mechanism to avoid undesired cell proliferation that plays a role in tumor suppression, wound healing and embryonic development. In order to gain insight on the evolution of senescence, we looked at its presence in developing axolotls (urodele amphibians) and in zebrafish (teleost fish), which are both anamniotes. Our data indicate that cellular senescence is present in various developing structures in axolotls (pronephros, olfactory epithelium of nerve fascicles, lateral organs, gums) and in zebrafish (epithelium of the yolk sac and in the lower part of the gut). Senescence was particularly associated with transient structures (pronephros in axolotls and yolk sac in zebrafish) suggesting that it may play a role in the elimination of these tissues. Our data supports the notion that cellular senescence evolved early in vertebrate evolution to influence embryonic development.

Senescence‐associated β‐galactosidase activity in the developing avian retina

“…More recently, it has also been shown to be a reliable method, with which the programmed cellular senescence was identified that occurs during embryonic development. [9][10][11][12][13][14][15][16] However, the present results demonstrate that the expression of cytochemically detectable β-galactosidase pH 6.0 activity is not limited to senescent cells since it was detected in subpopulations of differentiated retinal cells and in RPE cells. Indeed, in the literature, one finds that several authors have questioned whether SA-β-GAL is actually a reliable marker of cellular senescence in vivo and in vitro.…”

“…Its expression is detected in various embryonic tissues in narrow time windows in all the vertebrates analyzed so far from fish to mammals. [9][10][11][12][13][14][15][16] In all these studies, SA-β-GAL expression is usually linked with degenerating structures, and programmed cell senescence has been described as being accompanied by programmed cell death. Programmed cell death also plays a crucial role in the development of the vertebrate visual system.…”

“…Over the past few years, the view of senescence has been changed by the results of several studies, which have demonstrated that cellular senescence is essential for embryonic development (for a review, see Reference 9 ). In particular, it has been shown that senescence contributes to the remodeling of developing structures in mammals, [10][11][12] birds, [12][13][14] amphibians, 15,16 and fish. 16 In these models, cellular senescence is involved in the degeneration of embryonic structures, and this process is normally accompanied by apoptosis.…”

“…In particular, it has been shown that senescence contributes to the remodeling of developing structures in mammals, [10][11][12] birds, [12][13][14] amphibians, 15,16 and fish. 16 In these models, cellular senescence is involved in the degeneration of embryonic structures, and this process is normally accompanied by apoptosis. [11][12][13]15 The aforecited studies have detected abundant senescent cells during morphogenesis of the pronephros, mesonephros, neural tube, Wolffian duct, pharyngeal arches, and limbs.…”

Complementary and distinct roles of autophagy, apoptosis and senescence during early inner ear development

“…Specific SAβG staining was detected in the otic vesicle, neural roof plate, limb buds, and the mesonephros, among other locations. Although these phenotypes have been characterized in detail in mouse embryos, developmental senescence has also been identified in human, chick, quail, axolotl, xenopus and zebra fish embryos (Nacher et al, 2006;Muñoz-Espín et al, 2013;Storer et al, 2013;Lorda-Diez et al, 2015;Davaapil et al, 2017;Villiard et al, 2017), indicating that it represents an evolutionary conserved mechanism. Interestingly, physiological senescence has also been observed in the placenta, where it has been associated to trophoblast cell fusion (Chuprin et al, 2013), as well as in embryonically-derived membranes, where its dysregulation could be related to pregnancy and parturition defects (Cha and Aronoff, 2017).…”