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The electrophysiological properties of embryos Transfer

Award Number: R01HL175982
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 04/01/2025
PERIOD OF PERFORMANCE END DATE: 04/30/2028

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The electrophysiological properties of embryos Transfer - Project Summary Congenital heart disease (CHD) leads to severe morbidity and mortality in children in the US and worldwide. Despite this impact on child health, we simply do not understand the genetic causes of CHD. Indeed, we recently showed that ion channels play a critical role in CHD, LR patterning, and early germ layer specification. We previously outlined an ion channel signaling network where ERG channels suppress voltage-gated calcium channels and mTOR signaling enabling the exit from pluripotency to germ layer differentiation. However, this study raised several additional questions. For example, do the germ layers have different electrophysiological properties? What are the calcium-responsive transcription factors that activate mTOR signaling? The goal of this proposal is to answer these questions. We propose, and our preliminary data support, that ion channels define a new paradigm for cell signaling in early embryonic cells. Our data support an electrophysiological model where specific germ layer fates are dependent on an ion channel network. Our overarching hypothesis is that ion channels define electrical membrane potential and regulate voltage-gated Ca2+ channels that establish an exit from pluripotency towards specific cell fates, gastrulation, and LR patterning providing a plausible mechanism for our patients with Htx and CHD. Our electrophysiological pathway then integrates with biochemical signaling pathways that define specific cell fates in the embryo. In this proposal, we will focus on understanding the differences in electrical properties of the different germ layers using both electrophysiological measurements and gene knockdown in Xenopus. We will then also identify the transcription factors that regulate mTOR signaling in the early embryo. Our published results strongly point towards ETS and CRE transcription factors, and we will identify precisely which transcription factors play a key role in mTOR signaling and pluripotency. A major strength of our proposal is our expertise; we have forged a collaboration between Xenopus developmental biologists and electrophysiologists that will allow us to rigorously investigate membrane potential as an embryonic patterning mechanism.


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 = $612,607 )
2025	2025	CEDARS-SINAI MEDICAL CENTER	8700 BEVERLY BLVD	WEST HOLLYWOOD	CA	90048	LOS ANGELES	USA	Cardiovascular Diseases Research	001	2	8/15/2025	CHANGE OF GRANTEE / TRAINING INSTITUTION / AWARDING INSTITUTION	$612,607
2025	2024	YALE UNIV	150 MUNSON ST	NEW HAVEN	CT	06511	SOUTH CENTRAL CT	USA	Cardiovascular Diseases Research	000	1	8/15/2025	NEW	$0
														Subtotal = $612,607

Issue Date FY: 2024 ( Subtotal = $817,424 )
2024	2024	YALE UNIV	150 MUNSON ST	NEW HAVEN	CT	06511	SOUTH CENTRAL CT	USA	Cardiovascular Diseases Research	000	1	6/27/2024	NEW	$817,424
														Subtotal = $817,424

Grand Total All Awards = $1,430,031

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The electrophysiological properties of embryos Transfer

Award Number: R01HL175982

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 04/01/2025

PERIOD OF PERFORMANCE END DATE: 04/30/2028

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