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dictyNews

Electronic Edition

Volume 46, number 15

May 29, 2020



Please submit abstracts of your papers as soon as they have been

accepted for publication by sending them to [log in to unmask]

or by using the form at

http://dictybase.org/db/cgi-bin/dictyBase/abstract_submit.



Back issues of dictyNews, the Dicty Reference database and other

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=========

Abstracts

=========





Cell-substrate adhesion drives Scar/WAVE activation and phosphorylation, 

which controls pseudopod lifetime



Shashi Prakash Singh, Peter A. Thomason, Sergio Lilla,  Matthias Schaks, 

Qing Tang, Bruce L. Goode,  Laura M. Machesky,  Klemens Rottner,  

Robert H. Insall





PLOS Biology, accepted



The Scar/WAVE complex is the principal catalyst of pseudopod and 

lamellipod formation. Here we show that Scar/WAVE’s proline-rich domain 

is polyphosphorylated after the complex is activated. Blocking Scar/WAVE 

activation stops phosphorylation in both Dictyostelium and mammalian cells, 

implying that phosphorylation modulates pseudopods after they have been 

formed, rather than controlling whether they are initiated. Unexpectedly,

phosphorylation is not promoted by chemotactic signalling, but is greatly 

stimulated by cell:substrate adhesion and diminished when cells deadhere.

Phosphorylation-deficient or phosphomimetic Scar/WAVE mutants are both 

normally functional, and rescue the phenotype of knockout cells, 

demonstrating that phosphorylation is dispensable for activation and actin 

regulation. However, pseudopods and patches of phosphorylation-deficient 

Scar/WAVE last substantially longer in mutants, altering the dynamics and 

size of pseudopods and lamellipods, and thus changing migration speed. 

Scar/WAVE phosphorylation does not require ERK2, but the MAPKKK 

homologue SepA contributes substantially - sepA mutants have less steady-

state phosphorylation, which does not increase in response to adhesion. 

The mutants also behave similarly to cells expressing phosphorylation-

deficient Scar, with longer-lived pseudopods and patches of Scar recruitment. 

We conclude that pseudopod engagement with substratum is more important 

than extracellular signals at regulating Scar/WAVE’s activity, and that 

phosphorylation acts as a pseudopod timer, by promoting Scar/WAVE 

turnover.





submitted by:  Robert Insall   [[log in to unmask]]

——————————————————————————————————————





Conidial Melanin of the Human-Pathogenic Fungus Aspergillus 

fumigatus Disrupts Cell Autonomous Defenses in Amoebae



Iuliia Ferling, Joe Dan Dunn, Alexander Ferling, Thierry Soldati, 

Falk Hillmann





https://mbio.asm.org/content/11/3/e00862-20

DOI: 10.1128/mBio.00862-20



The human-pathogenic fungus Aspergillus fumigatus is a ubiquitous 

saprophyte that causes fatal lung infections in immunocompromised 

individuals. Following inhalation, conidia are ingested by innate immune cells 

and can arrest phagolysosome maturation. How this virulence trait could have 

been selected for in natural environments is unknown. Here, we found that 

surface exposure of the green pigment 1,8-dihydroxynaphthalene-(DHN)-

melanin can protect conidia from phagocytic uptake and intracellular killing by 

the fungivorous amoeba Protostelium aurantium and delays its exocytosis from 

the nonfungivorous species Dictyostelium discoideum. To elucidate the 

antiphagocytic properties of the surface pigment, we followed the antagonistic 

interactions of A. fumigatus conidia with the amoebae in real time. For both 

amoebae, conidia covered with DHN-melanin were internalized at far lower 

rates than were seen with conidia lacking the pigment, despite high rates of 

initial attachment to nonkilling D. discoideum. When ingested by D. discoideum, 

the formation of nascent phagosomes was followed by transient acidification of 

phagolysosomes, their subsequent neutralization, and, finally, exocytosis of the 

conidia. While the cycle was completed in less than 1 h for unpigmented 

conidia, the process was significantly prolonged for conidia covered with DHN-

melanin, leading to an extended intracellular residence time. At later stages of 

this cellular infection, pigmented conidia induced enhanced damage to 

phagolysosomes and infected amoebae failed to recruit the ESCRT (endosomal 

sorting complex required for transport) membrane repair machinery or the 

canonical autophagy pathway to defend against the pathogen, thus promoting 

prolonged intracellular persistence in the host cell and the establishment of a 

germination niche in this environmental phagocyte.





submitted by:  Falk Hillmann   [[log in to unmask]]

——————————————————————————————————————





Cytokinins in Dictyostelia – A unique model for studying the functions of 

signaling agents from species to kingdoms



Megan M. Aoki1*, R. J. N. Emery1, Christophe Anjard2,3,4, Craig R. Brunetti1, 

Robert J. Huber1



1 - Department of Biology, Trent University, Peterborough, Ontario, Canada

2 - UMR5306 Institut Lumière Matière (ILM), France

3 - Université Claude Bernard Lyon 1, France

4 - Université de Lyon, France





Frontiers in Cell and Developmental Biology, accepted



Cytokinins (CKs) are a diverse group of evolutionarily significant growth-

regulating molecules. While the CK biosynthesis and signaltransduction 

pathways are the most well-understood in plant systems, these molecules have 

been identified in all kingdoms of life.This review follows the recent discovery 

of an expanded CK profile in the social amoeba, Dictyostelium discoideum. A

comprehensive review on the present knowledge of CK biosynthesis, signal 

transduction, and CK-small molecule interactions within members of 

Dictyostelia will be summarized. In doing so, the utility of social amoebae will 

be highlighted as a model system for studying the evolution of these hormone-

like signaling agents, which will set the stage for future research in this area.





submitted by:  Megan Aoki   [[log in to unmask]]

==============================================================

[End dictyNews, volume 46, number 15]

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