dictyNews
Electronic Edition
Volume 35, number 5
August 13, 2010

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=========
Abstracts
=========


cAMP diffusion in Dictyostelium discoideum: A Green’s function method

Daniel S. Calovi, Leonardo G. Brunnet, and Rita M. C. de Almeida

Instituto de Física, Universidade Federal do Rio Grande do Sul, Av. 
Bento Gonçalves 9500, P.B. 15051, 91501-970 Porto Alegre, RS, 
Brazil


Physical review, E 82, 011909 2010

A Green’s function method is developed to approach the spatiotemporal 
equations describing the cAMP production in Dictyostelium discoideum, 
markedly reducing numerical calculations times: cAMP concentrations 
and gradients are calculated just at the amoeba locations. A single set 
of parameters is capable of reproducing the different observed behaviors, 
from cAMP synchronization, spiral waves and reaction-diffusion patterns 
to streaming and mound formation. After aggregation, the emergence 
of a circular motion of amoebas, breaking the radial cAMP field 
symmetry, is observed.


Submitted by  Daniel Calovi [calovi@if.ufrgs.br]
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The ROCO kinase QkgA is necessary for proliferation inhibition by 
autocrine signals in Dictyostelium discoideum 

Jonathan E. Phillips and Richard H. Gomer


Eukaryotic Cell, in press

AprA and CfaD are secreted proteins that function as autocrine signals 
to inhibit cell proliferation in Dictyostelium discoideum.  Cells lacking 
AprA or CfaD proliferate rapidly, and adding AprA or CfaD to cells 
slows proliferation. Cells lacking the ROCO kinase QkgA proliferate 
rapidly, with a doubling time 83% that of wild type, and overexpression 
of a QkgA-GFP fusion protein slows cell proliferation.  We found that 
qkgA¯ cells accumulate normal levels of extracellular AprA and CfaD.  
Exogenous AprA or CfaD does not slow the proliferation of cells lacking 
qkgA, and expression of QkgA-GFP in qkgA¯ cells rescues this 
insensitivity.  Like cells lacking AprA or CfaD, cells lacking QkgA tend 
to be multinucleate, accumulate nuclei rapidly, and show a mass and 
protein accumulation per nucleus like that of wild type, suggesting that 
QkgA negatively regulates proliferation but not growth.  Despite their 
rapid proliferation, cells lacking AprA, CfaD, or QkgA expand as a 
colony on bacteria less rapidly than wild type. Unlike AprA and CfaD, 
QkgA does not affect spore viability following multicellular development.  
Together, these results indicate that QkgA is necessary for proliferation 
inhibition by AprA and CfaD, that QkgA mediates some but not all of 
the effects of AprA and CfaD, and that QkgA may function downstream 
of these proteins in a signal transduction pathway regulating proliferation.   


Submitted by  Richard Gomer [rgomer@tamu.edu]
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[End dictyNews, volume 35, number 5]