dictyNews
Electronic Edition
Volume 38, number 7
March 2, 2012

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Abstracts
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Ca2+ signaling regulates ecmB expression, cell differentiation and 
slug regeneration in Dictyostelium

Yekaterina Poloz and Danton H. O’Day


Differentiation, in press

Ca2+ regulates cell differentiation and morphogenesis in a diversity of 
organisms and dysregulation of Ca2+ signal transduction pathways leads 
to many cellular pathologies. In Dictyostelium Ca2+ induces ecmB 
expression and stalk cell differentiation in vitro. Here we have analyzed 
the pattern of ecmB expression in intact and bisected slugs and the 
effect of agents that affect Ca2+ levels or antagonize calmodulin (CaM) 
on this expression pattern. We have shown that Ca2+ and CaM regulate 
ecmB expression and pstAB/pstB cell differentiation in vivo. Agents that 
increase intracellular Ca2+ levels increased ecmB expression and/or 
pstAB and pstB cell differentiation, while agents that decrease intracellular 
Ca2+ or antagonize CaM decreased it. In isolated slug tips agents that 
affect Ca2+ levels and antagonize CaM had differential effect on ecmB 
expression and cell differentiation in the anterior versus posterior zones. 
Agents that increase intracellular Ca2+ levels increased the number of 
ecmB expressing cells in the anterior region of slugs, while agents that 
decrease intracellular Ca2+ levels or antagonize CaM activity increased 
the number of ecmB expressing cells in the posterior. We have also 
demonstrated that agents that affect Ca2+ levels or antagonize CaM affect 
cells motility and regeneration of shape in isolated slug tips and backs and 
regeneration of tips in isolated slug backs. To our knowledge, this is the 
first study detailing the pattern of ecmB expression in regenerating slugs 
as well as the role of Ca2+ and CaM in the regeneration process and 
ecmB expression. 


Submitted by Danton H. O’Day [[log in to unmask]]
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A mechanosensory system governs myosin II accumulation in dividing cells

Kee YS, Ren Y, Dorfman D, Iijima M, Firtel RA, Iglesias PA, Robinson DN 


Mol. Biol. Cell 2012, in press. 

The mitotic spindle is generally considered the initiator of furrow ingression. 
However, recent studies suggest that furrows can form without spindles, 
particularly during asymmetric cell division. In Dictyostelium, the 
mechanoenzyme myosin II and the actin crosslinker cortexillin I form a 
mechanosensor that responds to mechanical stress, which could account 
for spindle-independent contractile protein recruitment. Here, we show that 
the regulatory and contractility network, composed of myosin II, cortexillin I, 
IQGAP2, kinesin-6 (kif12) and INCENP, is a mechanical stress-responsive 
system. Myosin II and cortexillin I form the core mechanosensor, and 
mechanotransduction is mediated by IQGAP2 to kif12 and INCENP. 
Additionally, IQGAP2 is antagonized by IQGAP1 to modulate the 
mechanoresponsiveness of the system, suggesting a possible mechanism 
for discriminating between mechanical and biochemical inputs.  Furthermore, 
IQGAP2 is important for maintaining spindle morphology and kif12 and 
myosin II cleavage furrow recruitment. Cortexillin II is not directly involved in 
myosin II mechanosensitive accumulation, but without cortexillin I, 
cortexillin II’s role in membrane-cortex attachment is revealed. Finally, the 
mitotic spindle is dispensable for the system. Overall, this mechanosensory 
system is structured like a control system characterized by mechanochemical 
feedback loops that regulate myosin II localization at sites of mechanical 
stress and the cleavage furrow.


Submitted by Douglas Robinson [[log in to unmask]]
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Deconvolution of the cellular force-generating subsystems that govern 
cytokinesis furrow ingression

Poirier C, Ng WP, Robinson DN, Iglesias PA.


PLoS Comp. Biol, in press.

Abstract: Cytokinesis occurs through the coordinated action of several 
biochemically-mediated stresses acting on the cytoskeleton. Here, we 
develop a computational model of cellularmechanics, and using a large 
number of experimentally measured biophysical parameters, we simulate 
cell division under a number of different scenarios. We demonstrate that 
traction-mediated protrusive forces or contractile forces due to myosin II 
are sufficient to initiate furrow ingression. Furthermore, we show that 
passive forces due to the cell’s cortical tension and surface curvature 
allow the furrow to complete ingression. We compare quantitatively the 
furrow thinning trajectories obtained from simulation with those observed 
experimentally in both wild-type and myosin II null Dictyostelium cells. 
Our simulations highlight the relative contributions of different 
biomechanical subsystems to cell shape progression during cell division.


Submitted by Douglas Robinson [[log in to unmask]]
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[End dictyNews, volume 38, number 7]