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The Role of skNAC in the Mechanically Induced Growth of Skeletal Muscle

Award Number: F32AR087772
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 06/01/2026
PERIOD OF PERFORMANCE END DATE: 05/31/2029

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The Role of skNAC in the Mechanically Induced Growth of Skeletal Muscle - Project Summary/Abstract The preservation of skeletal muscle mass is critical for maintaining quality of life and resilience against various diseases; however, effective interventions to maintain or increase muscle mass and thereby prevent physical decline are limited. Simply put, there is a critical need to identify signaling pathways that can promote muscle growth. Previous studies have established that mechanical signals are one of the most potent inducers of muscle growth, yet the underlying mechanisms remain far from understood. As such, the long-term goal of my research is to determine how mechanical signals regulate skeletal muscle mass. A longstanding paradigm asserts that an increase in mechanical loading leads to an mTORC1-dependent accumulation of newly synthesized proteins (NSPs) which, in turn, can induce both the radial and longitudinal growth of muscle fibers. However, our preliminary data demonstrate that while the radial growth of fibers is prevented by mTORC1 inhibition, the in- series addition of sarcomeres (i.e., longitudinal growth) is not. In an effort to identify the components of this mTORC1-independent pathway, our lab performed a phosphoproteome-wide analysis of the signaling events that occur in human skeletal muscle after two types of exercise: endurance exercise, which results in elevated aerobic capacity, and resistance exercise, which increases protein synthesis and muscle mass. Among the outcomes, we found that a protein called skNAC had 30 different sites that experienced a robust and sustained increase in phosphorylation specifically after resistance exercise. Follow-up studies in a mouse model of resistance exercise revealed that >98% of the sites phosphorylated on skNAC were mediated through an mTORC1-independent pathway. This was very intriguing because previous studies have indicated that skNAC can play a central role in the regulation of protein synthesis and sarcomerogenesis. Collectively, the aforementioned points led me to my central hypothesis: skNAC is a key component of an mTORC1-independent pathway that regulates the mechanically induced growth of skeletal muscle. To test this hypothesis, I will leverage a combination of cutting-edge imaging techniques, two distinct models of mechanically induced growth (myotenectomy and weight pulling), and recently developed methods for analyzing kinase-substrate interactions. These technologies, along with my newly minted skeletal muscle-specific and inducible skNAC knockout mouse, will enable me to test my hypothesis through the following aims: 1) Determine whether skNAC is necessary for the mechanically induced accumulation of NSPs at putative sites of growth; 2) Determine whether skNAC is necessary for the mechanically induced growth of skeletal muscle; 3) Identify the kinase(s) that promote the mechanically induced phosphorylation of skNAC. Collectively, the outcomes are expected to fill a major gap in our understanding of how mechanical signals regulate skeletal muscle mass and when combined with my personalized training plan, they will enable me to acquire the skills necessary to achieve my goal of becoming a principal investigator at a research-intensive institution.


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 = $82,000 )
2026	2026	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Arthritis, Musculoskeletal and Skin Diseases Research	001	1	7/8/2026	NEW	$0
2026	2026	UNIVERSITY OF WISCONSIN SYSTEM	21 N PARK ST STE 6301	MADISON	WI	53715	DANE	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	6/10/2026	NEW	$82,000
														Subtotal = $82,000

Grand Total All Awards = $82,000

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The Role of skNAC in the Mechanically Induced Growth of Skeletal Muscle

Award Number: F32AR087772

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 06/01/2026

PERIOD OF PERFORMANCE END DATE: 05/31/2029

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