A DNA replication-independent function of pre-replication complex genes during cell invasion in C. elegans.
Animals
Animals, Genetically Modified
Caenorhabditis elegans
/ cytology
Caenorhabditis elegans Proteins
/ genetics
Cell Cycle
/ genetics
Cell Movement
/ genetics
DNA Replication
/ genetics
Female
Gene Expression Profiling
/ methods
Gene Ontology
Larva
/ cytology
Phosphatidylinositol 3-Kinases
/ metabolism
Replication Origin
/ genetics
Signal Transduction
/ genetics
Vulva
/ cytology
Journal
PLoS biology
ISSN: 1545-7885
Titre abrégé: PLoS Biol
Pays: United States
ID NLM: 101183755
Informations de publication
Date de publication:
02 2022
02 2022
Historique:
received:
31
05
2021
accepted:
01
12
2021
entrez:
22
2
2022
pubmed:
23
2
2022
medline:
22
3
2022
Statut:
epublish
Résumé
Cell invasion is an initiating event during tumor cell metastasis and an essential process during development. A screen of C. elegans orthologs of genes overexpressed in invasive human melanoma cells has identified several components of the conserved DNA pre-replication complex (pre-RC) as positive regulators of anchor cell (AC) invasion. The pre-RC genes function cell-autonomously in the G1-arrested AC to promote invasion, independently of their role in licensing DNA replication origins in proliferating cells. While the helicase activity of the pre-RC is necessary for AC invasion, the downstream acting DNA replication initiation factors are not required. The pre-RC promotes the invasive fate by regulating the expression of extracellular matrix genes and components of the PI3K signaling pathway. Increasing PI3K pathway activity partially suppressed the AC invasion defects caused by pre-RC depletion, suggesting that the PI3K pathway is one critical pre-RC target. We propose that the pre-RC, or a part of it, acts in the postmitotic AC as a transcriptional regulator that facilitates the switch to an invasive phenotype.
Identifiants
pubmed: 35192608
doi: 10.1371/journal.pbio.3001317
pii: PBIOLOGY-D-21-01423
pmc: PMC8863262
doi:
Substances chimiques
Caenorhabditis elegans Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e3001317Subventions
Organisme : NIH HHS
ID : P40 OD010440
Pays : United States
Commentaires et corrections
Type : CommentIn
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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