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The CTNNBIP1-CLSTN1 fusion transcript regulates human neocortical development
Min-Yi Ou1, Qi Xiao2, Xiang-Chun Ju3
1School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China; Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China; University of Chinese Academy of Sciences, Beijing 100049, China.
Fusion transcripts play a key role in human brain development. This study identified novel fusion RNAs, including CTNNBIP1-CLSTN1, influencing neural progenitor cells and Wnt/β-catenin signaling, impacting cortex growth and evolution.
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Fusion transcripts are found in human tissues but their role in brain development is unknown.
- The developing neocortex is crucial for higher cognitive functions.
Purpose of the Study:
- To investigate the function of fusion transcripts during human brain development.
- To identify specific fusion transcripts involved in neural progenitor cell regulation and cortical patterning.
Main Methods:
- Analysis of RNA-sequence libraries from early to middle embryonic stages.
- Focus on CTNNBIP1-CLSTN1 (CTCL) fusion transcript in neural progenitors.
- Utilized human cerebral organoid models to study CTCL function.
Main Results:
- Identified 1,055 fusion transcripts in the developing neocortex.
- Discovered 98 fusion transcripts with distinct expression in neural progenitors and neurons.
- CTCL is enriched in outer radial glial cells and its downregulation impairs neural progenitor proliferation and promotes precocious neuronal differentiation.
- CTCL expression modulates Wnt/β-catenin signaling, affecting cortex patterning.
Conclusions:
- Fusion transcripts play significant roles in human brain development and evolution.
- CTNNBIP1-CLSTN1 is a key fusion transcript regulating neural progenitor dynamics and cortical development.
- Findings provide insights into the genetic mechanisms underlying human cortical expansion.
