umu.sePublikasjoner
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Epistasis studies reveal redundancy among calcium-dependent protein kinases in motility and invasion of malaria parasites
Vise andre og tillknytning
2018 (engelsk)Inngår i: Nature Communications, ISSN 2041-1723, E-ISSN 2041-1723, Vol. 9, artikkel-id 4248Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

In malaria parasites, evolution of parasitism has been linked to functional optimisation. Despite this optimisation, most members of a calcium-dependent protein kinase (CDPK) family show genetic redundancy during erythrocytic proliferation. To identify relationships between phospho-signalling pathways, we here screen 294 genetic interactions among protein kinases in Plasmodium berghei. This reveals a synthetic negative interaction between a hypomorphic allele of the protein kinase G (PKG) and CDPK4 to control erythrocyte invasion which is conserved in P. falciparum. CDPK4 becomes critical when PKG-dependent calcium signals are attenuated to phosphorylate proteins important for the stability of the inner membrane complex, which serves as an anchor for the acto-myosin motor required for motility and invasion. Finally, we show that multiple kinases functionally complement CDPK4 during erythrocytic proliferation and transmission to the mosquito. This study reveals how CDPKs are wired within a stage-transcending signalling network to control motility and host cell invasion in malaria parasites.

sted, utgiver, år, opplag, sider
Nature Publishing Group, 2018. Vol. 9, artikkel-id 4248
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-152977DOI: 10.1038/s41467-018-06733-wISI: 000447123000024PubMedID: 30315162OAI: oai:DiVA.org:umu-152977DiVA, id: diva2:1260248
Forskningsfinansiär
EU, Horizon 2020, 695596Tilgjengelig fra: 2018-11-01 Laget: 2018-11-01 Sist oppdatert: 2018-12-28bibliografisk kontrollert

Open Access i DiVA

fulltext(5993 kB)90 nedlastinger
Filinformasjon
Fil FULLTEXT01.pdfFilstørrelse 5993 kBChecksum SHA-512
3eafd4e19a18a559a2d89325a9a64585a856cf12d0e929f21cabf68d2fd47c22f9be5421f3d6703d63250d131edc63780d07d7d85a9eeb3c640a6075f69f9337
Type fulltextMimetype application/pdf

Andre lenker

Forlagets fulltekstPubMed

Personposter BETA

Billker, Oliver

Søk i DiVA

Av forfatter/redaktør
Gomes, Ana RitaBillker, OliverBrochet, Mathieu
Av organisasjonen
I samme tidsskrift
Nature Communications

Søk utenfor DiVA

GoogleGoogle Scholar
Totalt: 90 nedlastinger
Antall nedlastinger er summen av alle nedlastinger av alle fulltekster. Det kan for eksempel være tidligere versjoner som er ikke lenger tilgjengelige

doi
pubmed
urn-nbn

Altmetric

doi
pubmed
urn-nbn
Totalt: 167 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf