The Phenotyping Core (Core B) is designed to evaluate the functional properties of muscles, joints, and whole animals in animal models created by the various Center investigators or directly in human muscle. The Phenotyping Core will interface with the High Throughput Cell Sorting Core and the Imaging Core by helping Center investigators identify the appropriate functional evaluation of muscle, with special consideration of the specific manipulation created by the Center investigator. The quantitative functional evaluation conducted by the Phenotyping Core will often be combined with structural data obtained from the Imaging Core thereby providing possible mechanistic explanations for any functional effects that are found. Thus, the Phenotyping Core will provide accessibility to sophisticated physiological and biomechanical testing capabilities to all Center investigators.
The Specific Aims of the Phenotyping Core are: 1) To provide training and technical assistance in skeletal muscle identification, dissection and mounting for isolated contractile and metabolic studies of isolated muscles. 2) To provide training and technical assistance in developing specialized

Public Health Relevance

One of the great strengths of the Phenotyping Core are the multiple scale levels on which function can be assessed including the whole animal (on treadmills), whole joint (via torque motors), whole muscle (using in vitro testing) and isolated single fibers (also using in vitro testing). Thus, this Core plays an essential role in the proposed Center's long-term goal to achieve a comprehensive understanding of multi-scale structure function relationships in skeletal muscles. Since most of the devices in the core are highly specialized, they are generally unavailable to Center investigators, except through mechanisms such as the P30. This core thus fills a significant void in the local San Diego muscle research community.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
5P30AR061303-03
Application #
8532645
Study Section
Special Emphasis Panel (ZAR1-KM)
Project Start
Project End
Budget Start
2013-09-01
Budget End
2014-08-31
Support Year
3
Fiscal Year
2013
Total Cost
$255,231
Indirect Cost
$110,018
Name
University of California San Diego
Department
Type
DUNS #
804355790
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Chapman, Mark A; Pichika, Rajeswari; Lieber, Richard L (2015) Collagen crosslinking does not dictate stiffness in a transgenic mouse model of skeletal muscle fibrosis. J Biomech 48:375-8
Gokhin, David S; Tierney, Matthew T; Sui, Zhenhua et al. (2014) Calpain-mediated proteolysis of tropomodulin isoforms leads to thin filament elongation in dystrophic skeletal muscle. Mol Biol Cell 25:852-65
Dayanidhi, Sudarshan; Lieber, Richard L (2014) Skeletal muscle satellite cells: mediators of muscle growth during development and implications for developmental disorders. Muscle Nerve 50:723-32
Tierney, Matthew Timothy; Aydogdu, Tufan; Sala, David et al. (2014) STAT3 signaling controls satellite cell expansion and skeletal muscle repair. Nat Med 20:1182-6
Chakkalakal, Joe V; Christensen, Josef; Xiang, Wanyi et al. (2014) Early forming label-retaining muscle stem cells require p27kip1 for maintenance of the primitive state. Development 141:1649-59
Tuttle, Lori J; Alperin, Marianna; Lieber, Richard L (2014) Post-mortem timing of skeletal muscle biochemical and mechanical degradation. J Biomech 47:1506-9
Wahlquist, Christine; Jeong, Dongtak; Rojas-Muñoz, Agustin et al. (2014) Inhibition of miR-25 improves cardiac contractility in the failing heart. Nature 508:531-5
Chapman, Mark A; Zhang, Jianlin; Banerjee, Indroneal et al. (2014) Disruption of both nesprin 1 and desmin results in nuclear anchorage defects and fibrosis in skeletal muscle. Hum Mol Genet 23:5879-92
Albini, Sonia; Puri, Pier Lorenzo (2014) Generation of myospheres from hESCs by epigenetic reprogramming. J Vis Exp :e51243
Saccone, Valentina; Consalvi, Silvia; Giordani, Lorenzo et al. (2014) HDAC-regulated myomiRs control BAF60 variant exchange and direct the functional phenotype of fibro-adipogenic progenitors in dystrophic muscles. Genes Dev 28:841-57

Showing the most recent 10 out of 23 publications