Fak56's Role in Neuromuscular Junction Growth
Author Information
Author(s): Tsai Pei-I, Kao Hsiu-Hua, Grabbe Caroline, Lee Yu-Tao, Ghose Aurnab, Lai Tzu-Ting, Peng Kuan-Po, Van Vactor David, Palmer Ruth H, Chen Ruey-Hwa, Yeh Shih-Rung, Chien Cheng-Ting
Primary Institution: Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan
Hypothesis
Fak56 functions downstream of integrin alphaPS3betaν and suppresses MAPK activation in neuromuscular junction growth.
Conclusion
Fak56 is required to restrict neuromuscular junction growth during development and suppresses ERK activation.
Supporting Evidence
- Fak56 null mutants display overgrowth of larval neuromuscular junctions.
- Fak56 is required in presynapses to restrict NMJ growth.
- Fak56 downregulates ERK activity at NMJs.
- Reducing ERK activity suppresses Fak56 mutant NMJ phenotypes.
- Fak56 mediates signaling through the integrin receptor.
Takeaway
Fak56 helps control the growth of connections between nerve cells and muscles, making sure they don't grow too big.
Methodology
Generated mutants for the Drosophila FAK gene, Fak56, and analyzed neuromuscular junctions through immunostaining and genetic interactions.
Statistical Information
P-Value
0.026
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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