dictyNews
Electronic Edition
Volume 42, number 6
February 26, 2016

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Abstracts
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A Continuum Model of Transcriptional Bursting

Adam M Corrigan, Edward Tunnacliffe, Danielle Cannon, 
and Jonathan R Chubb*


Laboratory for Molecular Cell Biology and Division 
of Cell and Developmental Biology, University College London, 
Gower Street, London, WC1E 6BT.  


eLife, accepted

Transcription occurs in stochastic bursts. Early models based 
upon RNA hybridisation studies suggest bursting dynamics arise 
from alternating inactive and permissive states. Here we 
investigate bursting mechanism in live cells by quantitative 
imaging of actin gene transcription, combined with molecular 
genetics, stochastic simulation and probabilistic modelling. 
In contrast to early models, our data indicate a continuum of 
transcriptional states, with a slowly fluctuating initiation 
rate converting the gene between different levels of activity, 
interspersed with extended periods of inactivity. We place an 
upper limit of 40s on the lifetime of fluctuations in 
elongation rate, with initiation rate variations persisting 
an order of magnitude longer. TATA mutations reduce the 
accessibility of high activity states, leaving the lifetime 
of on- and off-states unchanged. A continuum or spectrum of 
gene states potentially enables a wide dynamic range for cell 
responses to stimuli.


submitted by: Jonathan Chubb [j.chubb@ucl.ac.uk]
———————————————————————————————————————


Differentiation-inducing factor 2 modulates chemotaxis via 
the histidine kinase DhkC-dependent pathway in Dictyostelium 
discoideum

Hidekazu Kuwayama, Yuzuru Kubohara

HK: Faculty of Life and Environmental Sciences, University 
of Tsukuba, Tsukuba 305-8572, Japan.
YK: Department of Health Science, Graduate School of Health 
and Sports Science, Juntendo University, Inzai 270-1695, Japan.


FEBS Letters, in press

DIF-1 and DIF-2 are signaling molecules that control chemotaxis 
in Dictyostelium discoideum. Whereas DIF-1 suppresses chemotaxis 
in shallow cAMP gradients, DIF-2 enhances chemotaxis under the 
same conditions via a phosphodiesterase, RegA, which is a part 
of the DhkC–RdeA–RegA two-component signaling system. In this 
study, to investigate the mechanism of the chemotaxis 
regulation by DIF-2, we examined the effects of DIF-2 
(and DIF-1) on chemotaxis in rdeA– and dhkC– mutant strains. 
In the parental wild-type strains, chemotactic cell movement 
was suppressed with DIF-1 and enhanced with DIF-2 in shallow 
cAMP gradients. In contrast, in both rdeA– and dhkC– strains, 
chemotaxis was suppressed with DIF-1 but unaffected by DIF-2. 
The results suggest that DIF-2 modulates chemotaxis via the 
DhkC–RdeA–RegA signaling system.


submitted by: Yuzuru Kubohara [ykuboha@juntendo.ac.jp]
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[End dictyNews, volume 42, number 6]