Biology subjects

Tseng, K.

Publications and source records attributed to Tseng, K..

3 recordsLinked to original sources

bioRxiv2025

A Conserved Mechanism in Eye Optical Development: Lens Nucleus Centralization in Xenopus laevis

Developing eye optics, determined by the lens and cornea, must coordinate with the axial length of growing eyes to focus light onto the retina to form an image. It was found that zebrafish (Danio rerio) lens nuclei are initially anteriorly localized in optical axes in larvae, then centralize at older stages. An anteriorly placed lens nucleus would increase lens power, thereby likely enabling a functional optical system in larvae, where eye axial length is short. To assess if alike mechanisms occur in other aquatic animals, we studied the clawed frog, Xenopus laevis, a fully aquatic species similarly relying on vision for survival at stages where eyes are small. We found the Xenopus tadpole lens nucleus also shifted from an anterior to a central location in the optical axis during the prometamorphosis period. Similarly, in eyes regenerated after embryonic ablation, tadpole lens nuclei are anteriorly localized then centralize before metamorphosis, recapitulating the same pattern as control developing eyes. Moreover, lens nuclei localization in optical axes in developing and regenerated Xenopus eyes show close correlations to axial eye length. Close correlation of these two parameters suggests lens nuclei centralization is required for a functional optical system by coordinating the focal length. Our findings suggest a conserved evolutionary mechanism for eye optical development in at least two aquatic species. Understanding key mechanisms regulating crosstalk between eye optics and eye axial length will aid in discovering mechanisms of optical development and future therapies to prevent or delay formation of refractive error when these two properties mismatch.

developmental biology↗

bioRxiv2024

Effects of early life adversity and adolescent basolateral amygdala inhibition on corticolimbic connectivity and anxiety behaviors

Early postnatal development of corticolimbic circuitry is shaped by the environment and is vulnerable to early life challenges. Prior work has shown that early life adversity (ELA) leads to hyperinnervation of glutamatergic basolateral amygdala (BLA) projections to the prefrontal cortex (PFC) in adolescence. While hyperinnervation is associated with later-life anxiety behaviors, the physiological changes underpinning corticolimbic and behavioral impacts of ELA are not understood. We tested whether postsynaptic BLA-driven PFC activity is enhanced in ELA-exposed animals, using the maternal separation (MS) model of ELA. PFC local-field potential following BLA stimulation was facilitated in MS-exposed adolescents. Since ELA increases activity of the early-developing BLA, while the PFC exhibits protracted development, we further examined impacts of glutamatergic BLA activity during early adolescence on later-life PFC innervation and heightened anxiety. In early adolescence, MS-exposed animals exhibited decreased anxiety-like behavior, and acute adolescent BLA inhibition induced behaviors that resembled those of MS animals. To examine long-lasting impacts of adolescent BLA activity on innervation, BLA-originating axonal boutons in the PFC were quantified in late adolescence after early adolescent BLA inhibition. We further tested whether late adolescent BLA-PFC changes were associated with anxious reactivity expressed as heightened acoustic startle responses. MS rearing increased BLA-PFC innervation and threat reactivity in late adolescence, however early adolescent BLA inhibition was insufficient to prevent MS effects, suggesting that earlier BLA activity or post-synaptic receptor rearrangement in the PFC drives altered innervation. Taken together, these findings highlight both pre- and postsynaptic changes in the adolescent BLA-PFC circuit following ELA.

neuroscience↗

bioRxiv2024

Notch is Required for Neural Progenitor Proliferation During Embryonic Eye Regrowth

The ability of an organism to regrow tissues is regulated by various signaling pathways. One such pathway that has been studied widely both in the context of regeneration and development is the Notch signaling pathway. Notch signaling is required for development of the eye and regeneration of tissues in multiple organisms but it is unknown if Notch plays a role in the regulation of Xenopus laevis embryonic eye regrowth. We found that Notch1 is required for eye regrowth and regulates retinal progenitor cell proliferation. Chemical and molecular inhibition of Notch1 significantly decreased eye regrowth through reducing retinal progenitor cell proliferation without affecting retinal differentiation. Temporal inhibition studies showed that Notch function is required during the first day of regrowth. Interestingly, Notch1 loss-of-function phenocopied the effects of the inhibition of the proton pump, V-ATPase, where retinal proliferation but not differentiation was blocked during eye regrowth. Overexpression of a form of activated Notch1, the Notch intracellular domain (NICD) was sufficient to rescue loss of eye regrowth due to V-ATPase inhibition, suggesting that Notch acts downstream of V-ATPase. These findings highlight the importance of the Notch signaling pathway in eye regeneration and its role in inducing retinal progenitor cell proliferation in response to injury.

developmental biology↗