User:Nikolai Slavov
Contact Info
- Nikolai Slavov
- van Oudenaarden Lab
- Massachusetts Institute of Technology, 68-359
- 77 Massachusetts Ave Cambridge, MA 02139
- http://mit.edu/nslavov/www/
- http://alum.mit.edu/www/nslavov
- Email me through OpenWetWare
Education
- 2010, PhD, Botstein Lab, Princeton University
- 2006, MS, Princeton University
- 2004, BS, Massachusetts Institute of Technology
Research interests
I am interested in the dynamics of cell growth, metabolic and regulatory processes during the eukaryotic cell division cycle (CDC), across a wide range of CDC periods. In particular, I study how the growth rate signal - which is function of the availability of nutrients and growth factors - regulates the switch between respiration and fermentation and changes the duration of phases of the cell growth and division cycles.
Publications
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Slavov, N., Carey, J., Linse S. (2013)
Calmodulin transduces Ca+2 oscillations into differential regulation of its target proteins
ACS Chemical Neuroscience, vol. 4, issue 2 PDF
The molecular and network properties of the calmodulin signaling network, combined with its lignad-binding dynamics, can transduce a common signal (calcium levels) through a common signaling hub (calmodulin) and yet send different signals to many downstream proteins.
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Slavov N. and Botstein D. (2012)
Decoupling Nutrient Signaling from Growth Rate Causes Aerobic Glycolysis and Deregulation of Cell Size and Gene Expression
Mol. Biol. Cell, vol. 24, no. 2 PDF
The nutrition and the growth rate of a cell are two interacting factors with pervasive physiological effects. Our experiments decouple these factors and demonstrate the role of a growth rate signal, independent of the actual rate of biomass increase, on gene regulation, the cell division cycle, and the switch to a respiro-fermentative metabolism.
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Slavov N., van Oudenaarden A.*(2012) How to Regulate a Gene: To Repress or to Activate? Mol. Cell, vol. 46, issue 5, 551-552
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Slavov N., Airoldi E., van Oudenaarden A., and Botstein D. (2012)
A Conserved Cell Growth Cycle Can Account for the Environmental Stress Responses of Divergent Eukaryotes
Mol. Biol. Cell, vol. 23, no. 10, 1986-1997 PDF
We find that transitions between the two phases of the cell growth cycle can account for the environmental stress response, the growth-rate response, and the cross protection between slow growth and various types of stress factors. We suggest that this mechanism is conserved across budding and fission yeast, and normal human cells.
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Slavov N., Macinskas J., Caudy A., Botstein D. (2011)
Metabolic Cycling without Cell Division Cycling in Respiring Yeast
PNAS, vol. 108, no. 47, 19090-19095 PDF
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Slavov N. and Botstein D. (2011)
Coupling among Growth Rate Response, Metabolic Cycle and Cell Division Cycle in Yeast
Mol. Biol. Cell, vol. 22, 1997-2009 PDF
We discovered that the relative durations of the phases of the yeast metabolic cycle change with the growth rate. These changes can explain mechanistically the transcriptional growth-rate responses of all yeast genes (25% of the genome) that we find to be the same across all studied nutrient limitations in either ethanol or glucose carbon source.
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Slavov N. (2010)
Inference of Sparse Networks with Unobserved Variables. Application to Gene Regulatory Networks, JMLR, vol. 9
- Silverman SJ, Petti AA, Slavov N, Parsons L, Briehof R, Thiberge SY, Zenklusen D, Gandhi SJ, Larson DR, Singer RH, and Botstein D. Metabolic cycling in single yeast cells from unsynchronized steady-state populations limited on glucose or phosphate. Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):6946-51. DOI:10.1073/pnas.1002422107 |
- Slavov N and Dawson KA. Correlation signature of the macroscopic states of the gene regulatory network in cancer. Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4079-84. DOI:10.1073/pnas.0810803106 |
Protocols
- Phosphate-Limited Medium with Ethanol as a Sole Source of Carbon and Energy[1]
- Glucose-Limited Mineral Medium[2]
- Ethanol-Limited Mineral Medium[3]