Tamara N. Alliston, Ph.D.

Scientific Director

Chief, Skeletal Mechanobiology Laboratory

Summary

Tamara N. Alliston, Ph.D., is the NIAMS Scientific Director and leads the NIAMS Intramural Research Program (IRP). In addition to planning, coordinating, and directing the NIAMS IRP's basic and scientific research programs, Dr. Alliston's key responsibilities include recruiting and retaining world-class investigators and charting the future direction of IRP research.

Before joining NIAMS, Dr. Alliston worked in progressively senior positions at the University of California San Francisco (UCSF), most recently as a Professor in the Department of Orthopaedic Surgery. At NIAMS, she leads an independent research program to identify multi-scale mechanisms of skeletal disease, which will build on the accomplishments of her laboratory in cell and tissue mechanobiology over the past twenty years.

Research Statement

My research studies the crosstalk between biochemical and physical cues in the skeleton. We identified mechanisms by which growth factors and transcription factors cooperate to direct skeletal cell differentiation and then showed that these pathways also specify key physical properties of the extracellular matrix and bone quality. We apply our expertise in studying TGFβ signaling to investigate the interaction between physical and biochemical signals in the control of skeletal cell function and the role of these pathways in skeletal disease using in vitro, in vivo, and computational models. 

Currently, we focus on the role of osteocytes in mechanometabolic coupling, whereby this head-to-toe network of mechanosensory cells balances energy intake and utilization to maintain metabolic and mechanical homeostasis. With a background that spans endocrinology, skeletal mechanobiology, and materials science, our research spans from the molecular to the organismal length scale. 

We embrace the creative use and development of new methods with the goal of understanding the role of musculoskeletal tissues in health, aging, and disease.

Scientific Publications

High-fat and high-carbohydrate diets increase bone fragility through TGF-β-dependent control of osteocyte function.

Dole NS, Betancourt-Torres A, Kaya S, Obata Y, Schurman CA, Yoon J, Yee CS, Khanal V, Luna CA, Carroll M, Salinas JJ, Miclau E, Acevedo C, Alliston T
JCI Insight.
2024 Jul 9;
9(16).
doi: 10.1172/jci.insight.175103
PMID: 39171528

Aging impairs the osteocytic regulation of collagen integrity and bone quality.

Schurman CA, Kaya S, Dole N, Luna NMM, Castillo N, Potter R, Rose JP, Bons J, King CD, Burton JB, Schilling B, Melov S, Tang S, Schaible E, Alliston T
Bone Res.
2024 Feb 26;
12(1).
doi: 10.1038/s41413-023-00303-7
PMID: 38409111

Osteocyte dysfunction promotes osteoarthritis through MMP13-dependent suppression of subchondral bone homeostasis.

Mazur CM, Woo JJ, Yee CS, Fields AJ, Acevedo C, Bailey KN, Kaya S, Fowler TW, Lotz JC, Dang A, Kuo AC, Vail TP, Alliston T
Bone Res.
2019;
7().
doi: 10.1038/s41413-019-0070-y
PMID: 31700695

Osteocyte-Intrinsic TGF-β Signaling Regulates Bone Quality through Perilacunar/Canalicular Remodeling.

Dole NS, Mazur CM, Acevedo C, Lopez JP, Monteiro DA, Fowler TW, Gludovatz B, Walsh F, Regan JN, Messina S, Evans DS, Lang TF, Zhang B, Ritchie RO, Mohammad KS, Alliston T
Cell Rep.
2017 Nov 28;
21(9).
doi: 10.1016/j.celrep.2017.10.115
PMID: 29186693

Discrete spatial organization of TGFβ receptors couples receptor multimerization and signaling to cellular tension.

Rys JP, DuFort CC, Monteiro DA, Baird MA, Oses-Prieto JA, Chand S, Burlingame AL, Davidson MW, Alliston TN
Elife.
2015 Dec 10;
4().
doi: 10.7554/eLife.09300
PMID: 26652004
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