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 """"""""jigs"""""""" and interfaces to measure joint or muscle torque, or to conduct whole animal funcfional measurements. 3) To provide technical assistance with snap-freezing and routine histological processing of skeletal muscle including hematoxylin and eosin, immunohistochemistry, quantitative morphometry, and qualitafive morphology. 4) To provide training and technical assistance in measuring various aspects of metabolism either in vivo of ex vivo in muscle.

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.

National Institute of Health (NIH)
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Center Core Grants (P30)
Project #
Application #
Study Section
Special Emphasis Panel (ZAR1)
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of California San Diego
La Jolla
United States
Zip Code
Madaro, Luca; Passafaro, Magda; Sala, David et al. (2018) Denervation-activated STAT3-IL-6 signalling in fibro-adipogenic progenitors promotes myofibres atrophy and fibrosis. Nat Cell Biol 20:917-927
Diez-Cuñado, Marta; Wei, Ke; Bushway, Paul J et al. (2018) miRNAs that Induce Human Cardiomyocyte Proliferation Converge on the Hippo Pathway. Cell Rep 23:2168-2174
Liu, Eva S; Martins, Janaina S; Zhang, Wanlin et al. (2018) Molecular analysis of enthesopathy in a mouse model of hypophosphatemic rickets. Development 145:
Sartorelli, Vittorio; Puri, Pier Lorenzo (2018) Shaping Gene Expression by Landscaping Chromatin Architecture: Lessons from a Master. Mol Cell 71:375-388
Marroncelli, Nicoletta; Bianchi, Marzia; Bertin, Marco et al. (2018) HDAC4 regulates satellite cell proliferation and differentiation by targeting P21 and Sharp1 genes. Sci Rep 8:3448
Gibbons, Michael C; Singh, Anshuman; Engler, Adam J et al. (2018) The role of mechanobiology in progression of rotator cuff muscle atrophy and degeneration. J Orthop Res 36:546-556
Gokhin, David S; Fowler, Velia M (2017) Software-based measurement of thin filament lengths: an open-source GUI for Distributed Deconvolution analysis of fluorescence images. J Microsc 265:11-20
Jordan, Sabine D; Kriebs, Anna; Vaughan, Megan et al. (2017) CRY1/2 Selectively Repress PPAR? and Limit Exercise Capacity. Cell Metab 26:243-255.e6
Roberts, Thomas C; Etxaniz, Usue; Dall'Agnese, Alessandra et al. (2017) BRD3 and BRD4 BET Bromodomain Proteins Differentially Regulate Skeletal Myogenesis. Sci Rep 7:6153
Latella, Lucia; Dall'Agnese, Alessandra; Boscolo, Francesca Sesillo et al. (2017) DNA damage signaling mediates the functional antagonism between replicative senescence and terminal muscle differentiation. Genes Dev 31:648-659

Showing the most recent 10 out of 86 publications