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Xenopus slc7a5 is essential for notochord function and eye development
Tomohisa Katada1, Hiroyuki Sakurai1
1Department of Pharmacology and Toxicology, Kyorin University School of Medicine, 6-20-2, Shinkawa, Mitaka, Tokyo 181-8611, Japan.
Abstract:
slc7a5 (also known as LAT1), largely accepted as an amino acid transporter, has been shown to play important roles in cancer and developmental processes. Because knockout mice of Slc7a5 are embryonically lethal due to placental defects, it is difficult to evaluate its role in early development. In this study, expression and function of slc7a5 were evaluated in Xenopus laevis embryos that develop without a placenta. Expression of slc7a5 was detected in the notochord and in the eye and it was not co-localized with slc3a2, which helps slc7a5 to localize at the plasma membrane, before the late neurula stage. Loss-of-function experiment with a morpholino antisense oligonucleotide led to defect of neural and non-neural patterning, inhibition of primary neurogenesis, and disruption of eye development. Disruption of neural development and primary neurogenesis was likely due to impaired notochord development as sonic hedgehog (shh) signaling pathway was compromised in slc7a5-inhibited embryos. These results suggest that slc7a5 is required for notochord development and subsequent primary neurogenesis via shh/gli signaling and for eye development. These novel developmental roles of slc7a5 appeared to be independent of transport function at least before the late neurula stage.
Insights
The amino acid transporter SLC7A5 (LAT1) is crucial for early development in Xenopus embryos, impacting notochord and eye formation independently of its transport function.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Solute carrier family 7 member 5 (SLC7A5), also known as LAT1, is recognized for its role in amino acid transport.
- Previous studies indicate SLC7A5 involvement in cancer and development, but its precise function in early embryogenesis is unclear due to embryonic lethality in mice.
- Xenopus laevis embryos offer a model to study placental-independent developmental processes.
Purpose of the Study:
- To investigate the expression and function of SLC7A5 in early Xenopus laevis development.
- To elucidate the role of SLC7A5 in neural patterning, neurogenesis, and eye development.
- To explore the potential involvement of SLC7A5 in the sonic hedgehog (Shh) signaling pathway during development.
Main Methods:
- Expression analysis of slc7a5 in Xenopus laevis embryos.
- Loss-of-function studies using morpholino antisense oligonucleotides targeting slc7a5.
- Assessment of neural and non-neural patterning, primary neurogenesis, eye development, and Shh signaling pathway activity.
Main Results:
- SLC7A5 expression was detected in the notochord and eye prior to the late neurula stage.
- Inhibition of slc7a5 resulted in defects in neural and non-neural patterning, primary neurogenesis, and eye development.
- Impaired notochord development and compromised Shh/Gli signaling were observed in slc7a5-inhibited embryos.
Conclusions:
- SLC7A5 is essential for notochord development and subsequent primary neurogenesis, mediated through the Shh/Gli signaling pathway.
- SLC7A5 plays a critical role in eye development.
- These developmental functions of SLC7A5 appear to be independent of its canonical amino acid transport activity in early embryonic stages.
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