#newsmayerlab — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #newsmayerlab, aggregated by home.social.
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On my way to Otsu, Japan, for the EMBO Workshop “Neurodevelopmental disorders: genes to circuits and behavior.” Looking forward to meeting colleagues, exchanging ideas, and presenting our lab’s latest work on how risk genes affect developmental gene regulation!
https://meetings.embo.org/event/26-neurodev-disorders
#Neurodevelopment #GeneRegulation #EMBO #newsmayerlab -
On my way to Otsu, Japan, for the EMBO Workshop “Neurodevelopmental disorders: genes to circuits and behavior.” Looking forward to meeting colleagues, exchanging ideas, and presenting our lab’s latest work on how risk genes affect developmental gene regulation!
https://meetings.embo.org/event/26-neurodev-disorders
#Neurodevelopment #GeneRegulation #EMBO #newsmayerlab -
On my way to Otsu, Japan, for the EMBO Workshop “Neurodevelopmental disorders: genes to circuits and behavior.” Looking forward to meeting colleagues, exchanging ideas, and presenting our lab’s latest work on how risk genes affect developmental gene regulation!
https://meetings.embo.org/event/26-neurodev-disorders
#Neurodevelopment #GeneRegulation #EMBO #newsmayerlab -
Our new review is out in European Journal of Neuroscience: “Decoding Brain Development and Function Through GABAergic Inhibitory Neurons.”
A real honor — and a lot of fun — to work on this with Renata Batista-Brito, Mercedes Paredes, and Carla G. Silva. A wonderful group of people to think about interneuron development with.
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Our new review is out in European Journal of Neuroscience: “Decoding Brain Development and Function Through GABAergic Inhibitory Neurons.”
A real honor — and a lot of fun — to work on this with Renata Batista-Brito, Mercedes Paredes, and Carla G. Silva. A wonderful group of people to think about interneuron development with.
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Our new review is out in European Journal of Neuroscience: “Decoding Brain Development and Function Through GABAergic Inhibitory Neurons.”
A real honor — and a lot of fun — to work on this with Renata Batista-Brito, Mercedes Paredes, and Carla G. Silva. A wonderful group of people to think about interneuron development with.
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Our new review is out in European Journal of Neuroscience: “Decoding Brain Development and Function Through GABAergic Inhibitory Neurons.”
A real honor — and a lot of fun — to work on this with Renata Batista-Brito, Mercedes Paredes, and Carla G. Silva. A wonderful group of people to think about interneuron development with.
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Our new review is out in European Journal of Neuroscience: “Decoding Brain Development and Function Through GABAergic Inhibitory Neurons.”
A real honor — and a lot of fun — to work on this with Renata Batista-Brito, Mercedes Paredes, and Carla G. Silva. A wonderful group of people to think about interneuron development with.
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Ann Rose Bright from our lab has received the Young Scientist Award of the MPI for Biological Intelligence, together with Inbal Shainer from the Baier lab.
Ann is honoured for her work on how the timing of neurogenesis shapes the development of GABAergic neurons. Inhibitory neurons are generated over a window of about a week, so neurons born towards the end have several days less to migrate, mature and form their connections than those born at the start. Ann found that late-born neurons mature faster, and identified the transcription factor NFIB as a central regulator of this stage-specific difference.
In Ann's words: "We found that late-born neurons catch up by maturing faster, with those born at the end of neurogenesis speeding up their whole developmental process to be ready in time."
Congratulations to Ann and to her co-first authors Yana Kotlyarenko and Florian Neuhaus. The prize is endowed by the Elisabeth und Helmut Uhl Stiftung.
Institute news: https://www.bi.mpg.de/news/2026-07-ysa
Paper, Nature Neuroscience: https://doi.org/10.1038/s41593-025-01999-y#newsmayerlab #YoungScientistAward #MaxPlanck #Neuroscience #Neurodevelopment
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Ann Rose Bright from our lab has received the Young Scientist Award of the MPI for Biological Intelligence, together with Inbal Shainer from the Baier lab.
Ann is honoured for her work on how the timing of neurogenesis shapes the development of GABAergic neurons. Inhibitory neurons are generated over a window of about a week, so neurons born towards the end have several days less to migrate, mature and form their connections than those born at the start. Ann found that late-born neurons mature faster, and identified the transcription factor NFIB as a central regulator of this stage-specific difference.
In Ann's words: "We found that late-born neurons catch up by maturing faster, with those born at the end of neurogenesis speeding up their whole developmental process to be ready in time."
Congratulations to Ann and to her co-first authors Yana Kotlyarenko and Florian Neuhaus. The prize is endowed by the Elisabeth und Helmut Uhl Stiftung.
Institute news: https://www.bi.mpg.de/news/2026-07-ysa
Paper, Nature Neuroscience: https://doi.org/10.1038/s41593-025-01999-y#newsmayerlab #YoungScientistAward #MaxPlanck #Neuroscience #Neurodevelopment
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Ann Rose Bright from our lab has received the Young Scientist Award of the MPI for Biological Intelligence, together with Inbal Shainer from the Baier lab.
Ann is honoured for her work on how the timing of neurogenesis shapes the development of GABAergic neurons. Inhibitory neurons are generated over a window of about a week, so neurons born towards the end have several days less to migrate, mature and form their connections than those born at the start. Ann found that late-born neurons mature faster, and identified the transcription factor NFIB as a central regulator of this stage-specific difference.
In Ann's words: "We found that late-born neurons catch up by maturing faster, with those born at the end of neurogenesis speeding up their whole developmental process to be ready in time."
Congratulations to Ann and to her co-first authors Yana Kotlyarenko and Florian Neuhaus. The prize is endowed by the Elisabeth und Helmut Uhl Stiftung.
Institute news: https://www.bi.mpg.de/news/2026-07-ysa
Paper, Nature Neuroscience: https://doi.org/10.1038/s41593-025-01999-y#newsmayerlab #YoungScientistAward #MaxPlanck #Neuroscience #Neurodevelopment
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Ann Rose Bright from our lab has received the Young Scientist Award of the MPI for Biological Intelligence, together with Inbal Shainer from the Baier lab.
Ann is honoured for her work on how the timing of neurogenesis shapes the development of GABAergic neurons. Inhibitory neurons are generated over a window of about a week, so neurons born towards the end have several days less to migrate, mature and form their connections than those born at the start. Ann found that late-born neurons mature faster, and identified the transcription factor NFIB as a central regulator of this stage-specific difference.
In Ann's words: "We found that late-born neurons catch up by maturing faster, with those born at the end of neurogenesis speeding up their whole developmental process to be ready in time."
Congratulations to Ann and to her co-first authors Yana Kotlyarenko and Florian Neuhaus. The prize is endowed by the Elisabeth und Helmut Uhl Stiftung.
Institute news: https://www.bi.mpg.de/news/2026-07-ysa
Paper, Nature Neuroscience: https://doi.org/10.1038/s41593-025-01999-y#newsmayerlab #YoungScientistAward #MaxPlanck #Neuroscience #Neurodevelopment
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Ann Rose Bright from our lab has received the Young Scientist Award of the MPI for Biological Intelligence, together with Inbal Shainer from the Baier lab.
Ann is honoured for her work on how the timing of neurogenesis shapes the development of GABAergic neurons. Inhibitory neurons are generated over a window of about a week, so neurons born towards the end have several days less to migrate, mature and form their connections than those born at the start. Ann found that late-born neurons mature faster, and identified the transcription factor NFIB as a central regulator of this stage-specific difference.
In Ann's words: "We found that late-born neurons catch up by maturing faster, with those born at the end of neurogenesis speeding up their whole developmental process to be ready in time."
Congratulations to Ann and to her co-first authors Yana Kotlyarenko and Florian Neuhaus. The prize is endowed by the Elisabeth und Helmut Uhl Stiftung.
Institute news: https://www.bi.mpg.de/news/2026-07-ysa
Paper, Nature Neuroscience: https://doi.org/10.1038/s41593-025-01999-y#newsmayerlab #YoungScientistAward #MaxPlanck #Neuroscience #Neurodevelopment
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Yesterday, the architectural design for our institute’s new research campus was presented. From my perspective, the concept looks really promising - thoughtfully crafted and quite inspiring.
https://www.bi.mpg.de/2026-07-neuer-campus
#newsmayerlab -
Yesterday, the architectural design for our institute’s new research campus was presented. From my perspective, the concept looks really promising - thoughtfully crafted and quite inspiring.
https://www.bi.mpg.de/2026-07-neuer-campus
#newsmayerlab -
Yesterday, the architectural design for our institute’s new research campus was presented. From my perspective, the concept looks really promising - thoughtfully crafted and quite inspiring.
https://www.bi.mpg.de/2026-07-neuer-campus
#newsmayerlab -
I’m very much looking forward to presenting our most recent work at the EMBO Workshop “Neurodevelopmental Disorders: Genes to Circuits and Behavior” in Japan this September.
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I’m very much looking forward to presenting our most recent work at the EMBO Workshop “Neurodevelopmental Disorders: Genes to Circuits and Behavior” in Japan this September.
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I’m very much looking forward to presenting our most recent work at the EMBO Workshop “Neurodevelopmental Disorders: Genes to Circuits and Behavior” in Japan this September.
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Genetic risk for neurodevelopmental and psychiatric disorders may act less by deleting inhibitory neuron types than by biasing how they are made. This is the subject of our new review in Current Opinion in Genetics & Development (Dvoretskova & Mayer).
We draw on developmental genetics, lineage tracing, and human genetics. The main point: disease-linked variants often don't abolish particular inhibitory neuron types. Instead they shift developmental trajectories — timing, fate bias, lineage allocation — leaving subtype proportions imbalanced among otherwise normal cell types.
https://doi.org/10.1016/j.gde.2026.102504
#newsmayerlab #neuroscience #neurodevelopment -
Genetic risk for neurodevelopmental and psychiatric disorders may act less by deleting inhibitory neuron types than by biasing how they are made. This is the subject of our new review in Current Opinion in Genetics & Development (Dvoretskova & Mayer).
We draw on developmental genetics, lineage tracing, and human genetics. The main point: disease-linked variants often don't abolish particular inhibitory neuron types. Instead they shift developmental trajectories — timing, fate bias, lineage allocation — leaving subtype proportions imbalanced among otherwise normal cell types.
https://doi.org/10.1016/j.gde.2026.102504
#newsmayerlab #neuroscience #neurodevelopment -
Genetic risk for neurodevelopmental and psychiatric disorders may act less by deleting inhibitory neuron types than by biasing how they are made. This is the subject of our new review in Current Opinion in Genetics & Development (Dvoretskova & Mayer).
We draw on developmental genetics, lineage tracing, and human genetics. The main point: disease-linked variants often don't abolish particular inhibitory neuron types. Instead they shift developmental trajectories — timing, fate bias, lineage allocation — leaving subtype proportions imbalanced among otherwise normal cell types.
https://doi.org/10.1016/j.gde.2026.102504
#newsmayerlab #neuroscience #neurodevelopment -
Genetic risk for neurodevelopmental and psychiatric disorders may act less by deleting inhibitory neuron types than by biasing how they are made. This is the subject of our new review in Current Opinion in Genetics & Development (Dvoretskova & Mayer).
We draw on developmental genetics, lineage tracing, and human genetics. The main point: disease-linked variants often don't abolish particular inhibitory neuron types. Instead they shift developmental trajectories — timing, fate bias, lineage allocation — leaving subtype proportions imbalanced among otherwise normal cell types.
https://doi.org/10.1016/j.gde.2026.102504
#newsmayerlab #neuroscience #neurodevelopment -
Genetic risk for neurodevelopmental and psychiatric disorders may act less by deleting inhibitory neuron types than by biasing how they are made. This is the subject of our new review in Current Opinion in Genetics & Development (Dvoretskova & Mayer).
We draw on developmental genetics, lineage tracing, and human genetics. The main point: disease-linked variants often don't abolish particular inhibitory neuron types. Instead they shift developmental trajectories — timing, fate bias, lineage allocation — leaving subtype proportions imbalanced among otherwise normal cell types.
https://doi.org/10.1016/j.gde.2026.102504
#newsmayerlab #neuroscience #neurodevelopment -
New preprint: "Stoichiometric transcription factor partnerships control GABAergic neuron fate allocation."
Cell identity in development is often described as a combinatorial transcription factor "code." We find it is also quantitative: not only which factors are present, but their relative abundance, can shape a cell's fate.
In the developing basal ganglia, a pool of undifferentiated progenitors gives rise to several GABAergic neuron types, including D1 and D2 medium spiny neurons. Using our in vivo clonal perturbation sequencing and clone2vec, we find that losing SP9 shifts the clonal fate bias of progenitors from D2 neurons toward other GABAergic fates.
The readout uses two modes of genome binding: at GC-rich promoters SP9 binds DNA directly and activates; at distal enhancers it binds indirectly, tethered by DLX, acting as a combinatorial repressor with the NuRD complex. When DLX is in excess it sequesters SP9 away from its activating targets, so a graded shift in the SP9:DLX ratio becomes a discrete fate choice. An SP9 variant linked to neurodevelopmental disorders impairs the activator mode.
With thanks to the team, collaborators, and to #SFARI, the #DFG and the #NLMFF.
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New preprint: "Stoichiometric transcription factor partnerships control GABAergic neuron fate allocation."
Cell identity in development is often described as a combinatorial transcription factor "code." We find it is also quantitative: not only which factors are present, but their relative abundance, can shape a cell's fate.
In the developing basal ganglia, a pool of undifferentiated progenitors gives rise to several GABAergic neuron types, including D1 and D2 medium spiny neurons. Using our in vivo clonal perturbation sequencing and clone2vec, we find that losing SP9 shifts the clonal fate bias of progenitors from D2 neurons toward other GABAergic fates.
The readout uses two modes of genome binding: at GC-rich promoters SP9 binds DNA directly and activates; at distal enhancers it binds indirectly, tethered by DLX, acting as a combinatorial repressor with the NuRD complex. When DLX is in excess it sequesters SP9 away from its activating targets, so a graded shift in the SP9:DLX ratio becomes a discrete fate choice. An SP9 variant linked to neurodevelopmental disorders impairs the activator mode.
With thanks to the team, collaborators, and to #SFARI, the #DFG and the #NLMFF.
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New preprint: "Stoichiometric transcription factor partnerships control GABAergic neuron fate allocation."
Cell identity in development is often described as a combinatorial transcription factor "code." We find it is also quantitative: not only which factors are present, but their relative abundance, can shape a cell's fate.
In the developing basal ganglia, a pool of undifferentiated progenitors gives rise to several GABAergic neuron types, including D1 and D2 medium spiny neurons. Using our in vivo clonal perturbation sequencing and clone2vec, we find that losing SP9 shifts the clonal fate bias of progenitors from D2 neurons toward other GABAergic fates.
The readout uses two modes of genome binding: at GC-rich promoters SP9 binds DNA directly and activates; at distal enhancers it binds indirectly, tethered by DLX, acting as a combinatorial repressor with the NuRD complex. When DLX is in excess it sequesters SP9 away from its activating targets, so a graded shift in the SP9:DLX ratio becomes a discrete fate choice. An SP9 variant linked to neurodevelopmental disorders impairs the activator mode.
With thanks to the team, collaborators, and to #SFARI, the #DFG and the #NLMFF.
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New preprint: "Stoichiometric transcription factor partnerships control GABAergic neuron fate allocation."
Cell identity in development is often described as a combinatorial transcription factor "code." We find it is also quantitative: not only which factors are present, but their relative abundance, can shape a cell's fate.
In the developing basal ganglia, a pool of undifferentiated progenitors gives rise to several GABAergic neuron types, including D1 and D2 medium spiny neurons. Using our in vivo clonal perturbation sequencing and clone2vec, we find that losing SP9 shifts the clonal fate bias of progenitors from D2 neurons toward other GABAergic fates.
The readout uses two modes of genome binding: at GC-rich promoters SP9 binds DNA directly and activates; at distal enhancers it binds indirectly, tethered by DLX, acting as a combinatorial repressor with the NuRD complex. When DLX is in excess it sequesters SP9 away from its activating targets, so a graded shift in the SP9:DLX ratio becomes a discrete fate choice. An SP9 variant linked to neurodevelopmental disorders impairs the activator mode.
With thanks to the team, collaborators, and to #SFARI, the #DFG and the #NLMFF.
-
New preprint: "Stoichiometric transcription factor partnerships control GABAergic neuron fate allocation."
Cell identity in development is often described as a combinatorial transcription factor "code." We find it is also quantitative: not only which factors are present, but their relative abundance, can shape a cell's fate.
In the developing basal ganglia, a pool of undifferentiated progenitors gives rise to several GABAergic neuron types, including D1 and D2 medium spiny neurons. Using our in vivo clonal perturbation sequencing and clone2vec, we find that losing SP9 shifts the clonal fate bias of progenitors from D2 neurons toward other GABAergic fates.
The readout uses two modes of genome binding: at GC-rich promoters SP9 binds DNA directly and activates; at distal enhancers it binds indirectly, tethered by DLX, acting as a combinatorial repressor with the NuRD complex. When DLX is in excess it sequesters SP9 away from its activating targets, so a graded shift in the SP9:DLX ratio becomes a discrete fate choice. An SP9 variant linked to neurodevelopmental disorders impairs the activator mode.
With thanks to the team, collaborators, and to #SFARI, the #DFG and the #NLMFF.
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I had a wonderful time visiting INMED in Marseille — many thanks to Stéphane Bugeon for the invitation.
I’m grateful for the opportunity to present our group’s research and for many inspiring conversations with the fantastic scientists there.
A great institute in a beautiful place!
#newsmayerlab -
I had a wonderful time visiting INMED in Marseille — many thanks to Stéphane Bugeon for the invitation.
I’m grateful for the opportunity to present our group’s research and for many inspiring conversations with the fantastic scientists there.
A great institute in a beautiful place!
#newsmayerlab -
I had a wonderful time visiting INMED in Marseille — many thanks to Stéphane Bugeon for the invitation.
I’m grateful for the opportunity to present our group’s research and for many inspiring conversations with the fantastic scientists there.
A great institute in a beautiful place!
#newsmayerlab -
New preprint from the lab!
How do brain progenitors choose between D1 and D2 medium spiny neurons? We find the *relative levels* of SP9 and DLX TFs tip the balance: SP9 activates D2 genes at promoters, and represses D1 enhancers via DLX/NuRD.
Proud of the team — combining sparse in vivo CRISPR, lineage barcoding, scRNA-seq, ChIP-seq, CUT&RUN and proteomics for mechanistic depth in in vivo functional genomics.
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New preprint from the lab!
How do brain progenitors choose between D1 and D2 medium spiny neurons? We find the *relative levels* of SP9 and DLX TFs tip the balance: SP9 activates D2 genes at promoters, and represses D1 enhancers via DLX/NuRD.
Proud of the team — combining sparse in vivo CRISPR, lineage barcoding, scRNA-seq, ChIP-seq, CUT&RUN and proteomics for mechanistic depth in in vivo functional genomics.
-
New preprint from the lab!
How do brain progenitors choose between D1 and D2 medium spiny neurons? We find the *relative levels* of SP9 and DLX TFs tip the balance: SP9 activates D2 genes at promoters, and represses D1 enhancers via DLX/NuRD.
Proud of the team — combining sparse in vivo CRISPR, lineage barcoding, scRNA-seq, ChIP-seq, CUT&RUN and proteomics for mechanistic depth in in vivo functional genomics.
-
New preprint from the lab!
How do brain progenitors choose between D1 and D2 medium spiny neurons? We find the *relative levels* of SP9 and DLX TFs tip the balance: SP9 activates D2 genes at promoters, and represses D1 enhancers via DLX/NuRD.
Proud of the team — combining sparse in vivo CRISPR, lineage barcoding, scRNA-seq, ChIP-seq, CUT&RUN and proteomics for mechanistic depth in in vivo functional genomics.
-
New preprint from the lab!
How do brain progenitors choose between D1 and D2 medium spiny neurons? We find the *relative levels* of SP9 and DLX TFs tip the balance: SP9 activates D2 genes at promoters, and represses D1 enhancers via DLX/NuRD.
Proud of the team — combining sparse in vivo CRISPR, lineage barcoding, scRNA-seq, ChIP-seq, CUT&RUN and proteomics for mechanistic depth in in vivo functional genomics.
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Excellent science and great discussions at the GOLGI III conference in Bordeaux. Many thanks to the organizers and everyone involved for a very engaging meeting in a close and collegial atmosphere. #newsmayerlab
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Excellent science and great discussions at the GOLGI III conference in Bordeaux. Many thanks to the organizers and everyone involved for a very engaging meeting in a close and collegial atmosphere. #newsmayerlab
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Excellent science and great discussions at the GOLGI III conference in Bordeaux. Many thanks to the organizers and everyone involved for a very engaging meeting in a close and collegial atmosphere. #newsmayerlab
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Excited to be in New York this week for the SFARI Investigator Meeting.
Looking forward to discussions on neurodevelopmental disorders, gene regulation, and developmental mechanisms — and to catching up with many colleagues and collaborators. #newsmayerlab
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Excited to be in New York this week for the SFARI Investigator Meeting.
Looking forward to discussions on neurodevelopmental disorders, gene regulation, and developmental mechanisms — and to catching up with many colleagues and collaborators. #newsmayerlab
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Excited to be in New York this week for the SFARI Investigator Meeting.
Looking forward to discussions on neurodevelopmental disorders, gene regulation, and developmental mechanisms — and to catching up with many colleagues and collaborators. #newsmayerlab
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Many thanks to Stéphanie Baulac and Bassem Hassan for hosting me at ICM and for the opportunity to present our lab’s work. Great discussions and a very enjoyable visit to Paris. #newsmayerlab
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Many thanks to Stéphanie Baulac and Bassem Hassan for hosting me at ICM and for the opportunity to present our lab’s work. Great discussions and a very enjoyable visit to Paris. #newsmayerlab
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Many thanks to Stéphanie Baulac and Bassem Hassan for hosting me at ICM and for the opportunity to present our lab’s work. Great discussions and a very enjoyable visit to Paris. #newsmayerlab
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Wrapping up 2025 with a small holiday get-together over dinner. Thanks to everyone who made this year inspiring. #newsmayerlab
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Wrapping up 2025 with a small holiday get-together over dinner. Thanks to everyone who made this year inspiring. #newsmayerlab
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Wrapping up 2025 with a small holiday get-together over dinner. Thanks to everyone who made this year inspiring. #newsmayerlab
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🎉 Congratulations to Ann Bright!
Our postdoc Ann Bright was invited to present her research at the 2025 SYNAPSES Symposium at Yale University — a prestigious and highly selective event showcasing outstanding postdoctoral neuroscientists from around the world.We’re proud to see her work recognized on this international stage! 👏
#Postdoc #SynapsesSymposium #NewsMayerlab -
🎉 Congratulations to Ann Bright!
Our postdoc Ann Bright was invited to present her research at the 2025 SYNAPSES Symposium at Yale University — a prestigious and highly selective event showcasing outstanding postdoctoral neuroscientists from around the world.We’re proud to see her work recognized on this international stage! 👏
#Postdoc #SynapsesSymposium #NewsMayerlab -
🎉 Congratulations to Ann Bright!
Our postdoc Ann Bright was invited to present her research at the 2025 SYNAPSES Symposium at Yale University — a prestigious and highly selective event showcasing outstanding postdoctoral neuroscientists from around the world.We’re proud to see her work recognized on this international stage! 👏
#Postdoc #SynapsesSymposium #NewsMayerlab -
Was the layered cortex really unique to amniotes? Salamanders, our anamniote cousins, suggest otherwise.
In a new preprint from Maria Antonietta Tosches’ lab (first author Astrid Deryckere), we show that salamanders share core developmental logic with mammals — but with an ancestral outside-in sequence.
Clonal lineage tracing in salamanders reveals that both superficial and deep-layer neurons arise from the same multipotent radial glia.
Glad to have contributed to this work.
#neuroscience #development #evolution #anamniotes #NewsMayerlab -
Was the layered cortex really unique to amniotes? Salamanders, our anamniote cousins, suggest otherwise.
In a new preprint from Maria Antonietta Tosches’ lab (first author Astrid Deryckere), we show that salamanders share core developmental logic with mammals — but with an ancestral outside-in sequence.
Clonal lineage tracing in salamanders reveals that both superficial and deep-layer neurons arise from the same multipotent radial glia.
Glad to have contributed to this work.
#neuroscience #development #evolution #anamniotes #NewsMayerlab -
Was the layered cortex really unique to amniotes? Salamanders, our anamniote cousins, suggest otherwise.
In a new preprint from Maria Antonietta Tosches’ lab (first author Astrid Deryckere), we show that salamanders share core developmental logic with mammals — but with an ancestral outside-in sequence.
Clonal lineage tracing in salamanders reveals that both superficial and deep-layer neurons arise from the same multipotent radial glia.
Glad to have contributed to this work.
#neuroscience #development #evolution #anamniotes #NewsMayerlab -
Was the layered cortex really unique to amniotes? Salamanders, our anamniote cousins, suggest otherwise.
In a new preprint from Maria Antonietta Tosches’ lab (first author Astrid Deryckere), we show that salamanders share core developmental logic with mammals — but with an ancestral outside-in sequence.
Clonal lineage tracing in salamanders reveals that both superficial and deep-layer neurons arise from the same multipotent radial glia.
Glad to have contributed to this work.
#neuroscience #development #evolution #anamniotes #NewsMayerlab -
🎉 Big congratulations to Yana Kotlyarenko for successfully defending her PhD!
She carried out her research project in our lab, and it’s been a joy to see her science and ideas grow. Wishing her all the best for the next steps! 🌟 -
🎉 Big congratulations to Yana Kotlyarenko for successfully defending her PhD!
She carried out her research project in our lab, and it’s been a joy to see her science and ideas grow. Wishing her all the best for the next steps! 🌟 -
🎉 Big congratulations to Yana Kotlyarenko for successfully defending her PhD!
She carried out her research project in our lab, and it’s been a joy to see her science and ideas grow. Wishing her all the best for the next steps! 🌟 -
We’ve updated the TrackerSeq pipeline on GitHub! Developed in our lab, TrackerSeq is a tool for processing lineage barcodes in single-cell datasets. Thanks to great work by Connor Lynch, cloneID assignment now uses a network-based approach with Jaccard distance weighting and user-controlled thresholding — reducing false positives while keeping true positives. https://github.com/mayer-lab/TrackerSeq