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This resulted in a decrease in the frequency of catastrophe for mal3Δ mtr1Δ cells.
mtr1p appears to increase the frequency of catastrophe, a role antagonistic to mal3p.
However, mtr1p appears to help increase microtubule growth velocity and to increase the frequency of catastrophe.
The β T238A mutation stimulated spontaneous nucleation and reduced the frequency of catastrophe and the rate of shrinking, all without substantially affecting elongation.
Further, the role of mtr1p in increasing the frequency of catastrophe is consistent with its role in decreasing the microtubule dwell-time.
The effect of mtr1-deletion on microtubule stability is relatively minor, with slight increase in dwell-time and slight decrease in the frequency of catastrophe.
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This allows us to predict how the evolutionary stable level of persisters depends upon population demographic parameters such as intensity of resource competition, the frequency of catastrophes such as antibiotic treatment, and the genetic structure (heterogeneity) of populations.
Early studies showed that depletion of kinesin-13 XKCM1 did not affect the rate of microtubule growth or shrinkage in extracts, but did result in a 4-fold decrease in the frequency of catastrophes (Walczak et al., 1996).
Conversely, overexpression of kinesin-13 in tissue culture cells leads to an increase in the frequency of catastrophes (Kline-Smith and Walczak, 2002) and a reduction in the number of microtubules (Maney et al, 1998), again consistent with kinesin-13 proteins being depolymerases in vivo.
The frequencies of catastrophe and rescue are important parameters in studying the dynamicity of microtubules.
At the plus ends, a class of MAPs termed the plus end tip tracking proteins (+TIPs) (Galjart, 2010) constitute the key players of the microtubule dynamics characterized by four parameters – velocities of growth and shrinkage, and frequencies of catastrophe and rescue, Vg, Vs, Fcat, Fres, respectively (Walker et al., 1988).
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