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Non-Autonomous Regulation of Interneuron Fate, Position, and Survival by Excitatory Neurons during Cortical Development

Award Number: F32NS148600
ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 12/01/2026
PERIOD OF PERFORMANCE END DATE: 11/30/2027

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Non-Autonomous Regulation of Interneuron Fate, Position, and Survival by Excitatory Neurons during Cortical Development - PROJECT SUMMARY Excitatory and inhibitory neurons establish precise patterns of connectivity during cortical development, and disruptions in excitatory-inhibitory balance are a hallmark of neurodevelopmental disorders such as autism spectrum disorder (ASD). Interneurons, which mediate inhibition in the cortex, are initially specified into a few cardinal classes during embryogenesis and are subsequently refined into dozens of transcriptionally distinct ‘definitive’ subtypes postnatally through a poorly understood process of fate refinement. Recent evidence suggests that non-autonomous cues from excitatory neurons play a key role in shaping cortical interneuron fate, position, and survival during embryonic and postnatal development—highlighting a critical window in which local interactions may influence long-term circuit organization. The primary goal of this NRSA F32 proposal is to define the spatial and temporal contributions of distinct excitatory neuron populations to interneuron development. I will focus on Tbr1 and Satb2, two transcription factors associated with ASD that regulate excitatory neuron identity in the cortex. Using Cre-conditional knockout approaches, I will test the hypothesis that excitatory neuron subtypes influence interneurons at discrete developmental stages leveraging single-nucleus RNA-seq and spatial transcriptomics. In Aim 1, I will knock out Tbr1 or Satb2 in early-born transient excitatory populations—Cajal-Retzius and subplate neurons— to assess their role in regulating interneuron fate and positioning during their migration. In Aim 2, I will knock out Tbr1 or Satb2 in layer-specific pyramidal neurons to test how changes in pyramidal neuron identity affects interneuron subtype fate and position. I will determine whether changes in subtype proportions relate to changes in cell survival by repeating key experiments under a Bax loss-of-function background, or cell fate, leveraging Waddington Optimal Transport and RNA velocity analysis to assess shifts in developmental trajectories. This work will be carried out in the laboratory of Dr. Gord Fishell at the Broad Institute—an outstanding training environment with deep expertise in developmental neuroscience. By linking subtype- and stage-specific excitatory-inhibitory interactions to genes implicated in ASD and ID, this work will advance our understanding of how early developmental perturbations alter circuit assembly and potentially contribute to neurodevelopmental disorders.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $76,780 )
2026	2026	THE BROAD INSTITUTE, INC	415 MAIN ST	CAMBRIDGE	MA	02142	MIDDLESEX	USA	Extramural Research Programs in the Neurosciences and Neurological Disorders	000	1	5/5/2026	NEW	$76,780
														Subtotal = $76,780

Grand Total All Awards = $76,780

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Non-Autonomous Regulation of Interneuron Fate, Position, and Survival by Excitatory Neurons during Cortical Development

Award Number: F32NS148600

ORGANIZATION: NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 12/01/2026

PERIOD OF PERFORMANCE END DATE: 11/30/2027

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