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Modulation of cone photoreceptor function by autophagy

Award Number: R01EY035137
ORGANIZATION: NATIONAL EYE INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 06/01/2023
PERIOD OF PERFORMANCE END DATE: 05/31/2027

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Modulation of cone photoreceptor function by autophagy - ABSTRACT Autophagy is a lysosomal degradation pathway that maintains cellular homeostasis under basal and stress conditions by catabolizing cellular constituents to produce energy and building blocks. Although autophagy is common to all eukaryotic cells, highly specialized cells exploit this pathway to support their unique physiological functions. One such example is cone photoreceptors, where autophagy promotes survival during periods of metabolic or light-induced stress. The function of cones as our daytime photoreceptors depends critically on the rapid recovery of their sensitivity after exposure to bright light, a process known as dark adaptation. This metabolically-demanding process is driven by the turnover of chromophore for the regeneration of cone visual pigment and by the resetting of the efficiency of synaptic transmission between cones and cone bipolar cells. As autophagy is intimately involved in cellular metabolism, we will test the novel hypothesis that autophagy modulates the cone-driven photopic dark adaptation. We will perform experiments to determine the physiological conditions that activate autophagy in cones, focusing on bright light exposure, fasting, and physical exercise. We will also determine the subcellular compartments in cones where autophagy is upregulated in response to a range of stress conditions. To investigate the role of autophagy in cone-driven photopic dark adaptation, we will perform electrophysiological experiments to determine how fasting, exercise, or genetic block of autophagy affect the recovery of photopic function following exposure to bright light. Finally, we will evaluate two alternative mechanisms by which autophagy could be modulating photopic dark adaptation, either by accelerating the turnover of visual chromophore or by enhancing synaptic transmission. These experiments will establish autophagy as a novel mechanism for regulating the function of mammalian cone photoreceptors and photopic vision. They will also pave the way for future translational studies with humans seeking to prevent vision loss and enhance photopic vision by intermittent fasting or exercise.


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: 2025 ( Subtotal = $394,205 )
2025	2025	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Vision Research	000	3	7/28/2025	NON-COMPETING CONTINUATION	$394,205
														Subtotal = $394,205

Issue Date FY: 2024 ( Subtotal = $396,943 )
2024	2024	UNIVERSITY OF CALIFORNIA IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Vision Research	000	2	6/13/2024	NON-COMPETING CONTINUATION	$396,943
														Subtotal = $396,943

Issue Date FY: 2023 ( Subtotal = $412,900 )
2023	2023	UNIVERSITY OF CALIFORNIA, IRVINE	160 ALDRICH HALL	IRVINE	CA	92697	ORANGE	USA	Vision Research	000	1	5/23/2023	NEW	$412,900
														Subtotal = $412,900

Grand Total All Awards = $1,204,048

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Modulation of cone photoreceptor function by autophagy

Award Number: R01EY035137

ORGANIZATION: NATIONAL EYE INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 06/01/2023

PERIOD OF PERFORMANCE END DATE: 05/31/2027

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