Patryk Poliński
@ppolinski.bsky.social
Postdoc at @EMBLBarcelona. Working on unusual forms of splicing.
Expansion of: nature.com/articles/s41...
June 10, 2025 at 7:20 AM
Expansion of: nature.com/articles/s41...
Thanks a lot Arnau!
May 10, 2025 at 7:47 AM
Thanks a lot Arnau!
Summarizing, we discovered that a neural-specific microexon in DAAM1 is a novel regulatory mechanism of actin cytoskeleton dynamics, which is necessary for proper memory formation and learning in mammals.
Thank you to everyone involved for putting this together!
Thank you to everyone involved for putting this together!
May 9, 2025 at 9:35 AM
Summarizing, we discovered that a neural-specific microexon in DAAM1 is a novel regulatory mechanism of actin cytoskeleton dynamics, which is necessary for proper memory formation and learning in mammals.
Thank you to everyone involved for putting this together!
Thank you to everyone involved for putting this together!
The last step was to perform rescue experiments.
Excitingly, treatment with a ROCK inhibitor partially rescued observed phenotypes, including learning deficits!
Excitingly, treatment with a ROCK inhibitor partially rescued observed phenotypes, including learning deficits!
May 9, 2025 at 9:35 AM
The last step was to perform rescue experiments.
Excitingly, treatment with a ROCK inhibitor partially rescued observed phenotypes, including learning deficits!
Excitingly, treatment with a ROCK inhibitor partially rescued observed phenotypes, including learning deficits!
Next, we investigated in detail the molecular mechanism of the observed phenotypes.
One of the leads guided us to increased RHOA/ROCK signaling in KO neurons! RhoA is a direct interactor of Daam1, whose activity is commonly associated with the number of “learning spines”.
One of the leads guided us to increased RHOA/ROCK signaling in KO neurons! RhoA is a direct interactor of Daam1, whose activity is commonly associated with the number of “learning spines”.
May 9, 2025 at 9:35 AM
Next, we investigated in detail the molecular mechanism of the observed phenotypes.
One of the leads guided us to increased RHOA/ROCK signaling in KO neurons! RhoA is a direct interactor of Daam1, whose activity is commonly associated with the number of “learning spines”.
One of the leads guided us to increased RHOA/ROCK signaling in KO neurons! RhoA is a direct interactor of Daam1, whose activity is commonly associated with the number of “learning spines”.
With help from @maradierssen.bsky.social, we found that DAAM1-MIC KO reduced long-term potentiation (LTP) in hippocampal neurons.
Moreover, dendritic spine analysis by @eloisaherrera.bsky.social revealed defects mainly in postsynaptic regions and a significant decrease in thin "learning spines."
Moreover, dendritic spine analysis by @eloisaherrera.bsky.social revealed defects mainly in postsynaptic regions and a significant decrease in thin "learning spines."
May 9, 2025 at 9:35 AM
With help from @maradierssen.bsky.social, we found that DAAM1-MIC KO reduced long-term potentiation (LTP) in hippocampal neurons.
Moreover, dendritic spine analysis by @eloisaherrera.bsky.social revealed defects mainly in postsynaptic regions and a significant decrease in thin "learning spines."
Moreover, dendritic spine analysis by @eloisaherrera.bsky.social revealed defects mainly in postsynaptic regions and a significant decrease in thin "learning spines."
Yet, the most exciting part began when we generated genetically engineered DAAM1-MIC KO mice!
We performed multiple assays to evaluate animal behavior. Strikingly, they showed clear learning impairments after microexon removal. What are the cellular and molecular bases for this?
We performed multiple assays to evaluate animal behavior. Strikingly, they showed clear learning impairments after microexon removal. What are the cellular and molecular bases for this?
May 9, 2025 at 9:35 AM
Yet, the most exciting part began when we generated genetically engineered DAAM1-MIC KO mice!
We performed multiple assays to evaluate animal behavior. Strikingly, they showed clear learning impairments after microexon removal. What are the cellular and molecular bases for this?
We performed multiple assays to evaluate animal behavior. Strikingly, they showed clear learning impairments after microexon removal. What are the cellular and molecular bases for this?