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An Eye in the Replication Stress Response: Lessons From Tissue-Specific Studies in vivo.
Gabriel E Matos-Rodrigues1, Rodrigo A P Martins1
1Programa de Biologia Celular e do Desenvolvimento, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Frontiers in Cell and Developmental Biology
|November 22, 2021
Summary
Mutations in replication stress response (RSR) genes cause human syndromes. Different cell types show varied responses to RSR inactivation, impacting eye development and disease mechanisms.
Area of Science:
- Developmental Biology
- Genetics
- Cell Biology
Background:
- Inherited human syndromes affecting organogenesis are linked to mutations in replication stress response (RSR) genes.
- RSR molecular machinery is conserved, but mutations can lead to distinct tissue-specific outcomes.
- Understanding cell-type-specific responses to replication stress is key to RSR-related human syndromes.
Purpose of the Study:
- To review ocular manifestations in RSR-related human syndromes.
- To summarize current research on RSR mechanisms during *in vivo* eye development.
- To highlight progenitor cell response heterogeneity to RSR inactivation.
Main Methods:
- Literature review of RSR-related human syndromes.
- Analysis of *in vivo* studies on RSR during eye development.
- Comparative analysis of progenitor cell responses to RSR inactivation.
Main Results:
- Ocular manifestations are common in RSR-related human syndromes.
- Progenitor cells exhibit significant heterogeneity in their response to RSR gene inactivation.
- This heterogeneity influences the mechanisms underlying RSR-related human syndromes.
Conclusions:
- Replication stress response (RSR) plays a critical role in eye development.
- Varied progenitor cell responses to RSR inactivation contribute to the diverse clinical outcomes of RSR-related syndromes.
- Targeting these cell-specific responses may offer therapeutic avenues for RSR-related human syndromes.
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