One scientific question that excites me the most is how changes in metabolism can alter the propensity of a cell to commit to a specific lineage. For instance, are there metabolism-dependent mechanisms that determine whether a progenitor cell commits to becoming a fat cell instead of a muscle cell? Or even more fundamentally, early on in development – could metabolic changes underlie cell fate commitments that underpin our subsequent development?
This is an emerging topic that has been embraced by several groups across the globe. Most recently, I came across aReview in Genetics & Development that deals with the exact same question: Metabolic switching and cell fate decisions: implications for pluripotency, reprogramming and development (Cliff, T & Dalton, S; 2017)
This prompted me to dig back in my library for other papers and reviews on the topic in case others out there might find it useful. Below is a non-comprehensive list that also includes several tangentially relevant inputs from the cancer field (also, note the list of papers referenced in the above review):
- Vander Heiden, M. et al. (2009, Science): Understanding the Warburg effect: cell proliferation
- Folmes et al. (2011, Cell Metabolism): Somatic oxidative bioenergetics transitions into pluripotency-dependent glycolysis to facilitate nuclear reprogramming.
- Varum et al. (2011, PLoS One): Energy metabolism in human pluripotent stem cells and their differentiated counterparts.
- Zhang et al. (2012, Cell Stem Cell): Metabolic regulation in pluripotent stem cells during reprogramming and self-renewal.
- Folmes et al. (2012, Cell Stem Cell): Metabolic plasticity in stem cell homeostasis and differentiation.
- Metallo, C. & Vander Heiden, M. (2013, Molecular Cell): Understanding metabolic regulation and its influence on cell physiology.
- Ito, K. & Suda, T. (2014, Nature Reviews Molecular Cell Biology): Metabolic requirements for the maintenance of self-renewing stem cells.
- Badur et al. (2015, Biotechnology Journal): Enzymatic passaging of human embryonic stem cells alters central carbon metabolism and glycan abundance.
- Menendez, J. (2015): Metabolic control of cancer cell stemness: Lessons from iPS cells.
- Qian et al. (2015, Cell Stem Cell): The Dlk1-Gtl2 locus preserve LT-HSC function by inhibiting the PI3K-mTOR pathway to restrict mitochondrial metabolism.
- Wu et al. (2016, Cell): Cellular metabolism and induced pluripotency.
- Chandel et al. (2016, Nature Cell Biology): Metabolic regulation of stem cell function in tissue homeostasis and organismal ageing.
- Yu, J. & Cui, W. (2016, Development): Proliferation, survival and metabolism: the role of PI3K/AKT/mTOR signalling in pluripotency and cell fate determination.
- Adams et al. (2016, Cell Reports): Anabolism-associated mitochondrial stasis driving lymphocyte differentiation over self-renewal.
- Gu et al. (2016, Cell Stem Cell): Glycolytic Metabolism Plays a Functional Role in Regulating Human Pluripotent Stem Cell State.
- Ho et al. (2017, Nature): Autophagy maintains the metabolism and function of young and old stem cells.
- Anso et al. (2017, Nature Cell Biology): The mitochondrial respiratory chain is essential for haematopoietic stem cell function.
- Shell, J & Rutter, J (2017, Nature Cell Biology) ➡ commentary on (2): Mitochondria link metabolism and epigenetics in haematopoiesis.
- Cha et al. (2017, Nature Cell Biology): Metabolic control of primed human pluripotent stem cell fate and function by the miR-200c-SIRT2 axis.
- Yu et al. (2017, Nature): FGF-dependent metabolic control of vascular development.
- Sone et al. (2017, Cell Metabolism): Hybrid cellular metabolism coordinated by Zic3 and Esrrb synergistically enhances induction of naive pluripotency.
- Vander Heiden, M. & DeBerardinis, R. (2017, Cell): Understanding the intersections between metabolism and cancer biology.