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Elucidating the role of SAMD7 in photoreceptor transcriptional regulation.

Award Number: F30EY038618
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 06/04/2026
PERIOD OF PERFORMANCE END DATE: 09/03/2029

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Elucidating the role of SAMD7 in photoreceptor transcriptional regulation. - PROJECT SUMMARY/ABSTRACT Understanding the mechanisms governing cell-type specific gene expression in the retina is essential for elucidating developmental processes, uncovering the basis of degenerative disorders, and guiding reprogramming-based therapies for blinding diseases. Transcription factors (TFs) play a crucial role in coordinating the diverse transcriptional programs across cell types, but many key transcriptional regulators lack DNA-binding domains and function through interactions with effectors and chromatin regulators facilitated through intrinsically disordered regions (IDRs). This proposal investigates the role of Samd7, a photoreceptor-specific protein that contains a large IDR, in regulating gene expression. Samd7 serves to repress cone genes in mouse retina by serving as a molecular bridge between Nr2e3 and the Polycomb Repressive Complex 1 (PRC1). By dissecting the interplay between Samd7, the rod transcription factor Nr2e3, and the (PRC1) in the context of photoreceptor gene regulation, this project will establish the molecular mechanisms by which non-DNA binding transcriptional regulators confer specificity to cell-type specific gene expression programs. Specifically, I will use RNA- and ATAC-seq to identify Samd7 target genes and regulatory elements in rods and cone subtypes. Using genomic profiling techniques, I will assess a hierarchical model where Nr2e3 recruits Samd7 to repressed cone genes, and Samd7, in turn, recruits PRC1 to carry out gene repression. Finally, I will characterize the molecular interfaces governing Samd7-Nr2e3 interactions through computational modeling and yeast two-hybrid assays, providing mechanistic insights into how IDR-containing proteins contribute to photoreceptor identity. The integrated research design combines transgenic mouse models of the retina, multi-omics approaches, and computational modeling to address critical gaps in our understanding of photoreceptor gene regulation and mechanisms of transcriptional control that drive cell identity. This work not only promises to advance fundamental biology but also holds potential to inform reprogramming-based therapeutic approaches. This fellowship will provide rigorous training in the mouse retina, chromatin biology and transcriptional regulation, computational genomics, and intrinsically disordered protein biophysics. I will be supported by a synergistic co-mentorship of Dr. Joseph Corbo and Dr. Alex Holehouse, leaders in the fields of photoreceptor gene regulation and intrinsically disordered proteins, respectively. I am additionally supported by world-class research infrastructure and exceptionally strong training programs in Computational Biology, Visual Sciences, and Biochemistry.


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 = $37,249 )
2026	2026	WASHINGTON UNIVERSITY, THE	1 BROOKINGS DR	SAINT LOUIS	MO	63130	SAINT LOUIS	USA	Vision Research	001	1	4/21/2026	NEW	$0
2026	2026	WASHINGTON UNIVERSITY, THE	1 BROOKINGS DR	SAINT LOUIS	MO	63130	SAINT LOUIS	USA	Vision Research	000	1	4/21/2026	NEW	$37,249
														Subtotal = $37,249

Grand Total All Awards = $37,249

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Elucidating the role of SAMD7 in photoreceptor transcriptional regulation.

Award Number: F30EY038618

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 06/04/2026

PERIOD OF PERFORMANCE END DATE: 09/03/2029

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