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Loss of growth homeostasis by genetic decoupling of cell division from biomass growth: implication for size control mechanisms.

Schmidt-Glenewinkel H, Barkai N - Mol. Syst. Biol. (2014)

Bottom Line: This was achieved by modulating glucose influx independently of external glucose.Division rate followed glucose influx, while volume growth was largely defined by external glucose.We present a class of size control models explaining the observed breakdowns of growth homeostasis.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

No MeSH data available.


Glucose influx modulates cell division independently of external glucose
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fig02: Glucose influx modulates cell division independently of external glucose

Mentions: We expressed the mid-affinity glucose transporter HXT2 (Reifenberger et al, 1997; Fuhrmann et al, 1998) (Km ∼10 mM), driven by the TET promoter, in the transporterless strain. This allowed us to modulate glucose influx while keeping external glucose constant by adding doxycycline (DOX) (Fig2A). Aspects of growth that depend only on external signals will not be modulated by the change in glucose influx. In contrast, aspects that depend on glucose influx will be modulated by changing DOX, while maintaining external glucose constant. We fixed external glucose at intermediate levels (0.1%) and tested the effect of adding different DOX levels on cell size and cell division. Steady-state growth was retrieved for DOX levels ≥ 250 ng. Division rate increased with increasing DOX, indicating that glucose influx directly controls division rate (Fig2B). Cells reached wild-type division rate at the maximal DOX tested (Fig2B). Notably, cell size decreased in proportion with the increasing DOX levels, resulting in an inverse correlation between cell size and division rate. This inverse correlation contrasts the characteristic positive coordination between cell size, cell division, and glucose levels, observed during normal wild-type growth (c.f. Fig1C).


Loss of growth homeostasis by genetic decoupling of cell division from biomass growth: implication for size control mechanisms.

Schmidt-Glenewinkel H, Barkai N - Mol. Syst. Biol. (2014)

Glucose influx modulates cell division independently of external glucose
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4300492&req=5

fig02: Glucose influx modulates cell division independently of external glucose
Mentions: We expressed the mid-affinity glucose transporter HXT2 (Reifenberger et al, 1997; Fuhrmann et al, 1998) (Km ∼10 mM), driven by the TET promoter, in the transporterless strain. This allowed us to modulate glucose influx while keeping external glucose constant by adding doxycycline (DOX) (Fig2A). Aspects of growth that depend only on external signals will not be modulated by the change in glucose influx. In contrast, aspects that depend on glucose influx will be modulated by changing DOX, while maintaining external glucose constant. We fixed external glucose at intermediate levels (0.1%) and tested the effect of adding different DOX levels on cell size and cell division. Steady-state growth was retrieved for DOX levels ≥ 250 ng. Division rate increased with increasing DOX, indicating that glucose influx directly controls division rate (Fig2B). Cells reached wild-type division rate at the maximal DOX tested (Fig2B). Notably, cell size decreased in proportion with the increasing DOX levels, resulting in an inverse correlation between cell size and division rate. This inverse correlation contrasts the characteristic positive coordination between cell size, cell division, and glucose levels, observed during normal wild-type growth (c.f. Fig1C).

Bottom Line: This was achieved by modulating glucose influx independently of external glucose.Division rate followed glucose influx, while volume growth was largely defined by external glucose.We present a class of size control models explaining the observed breakdowns of growth homeostasis.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.

No MeSH data available.