OSCR

aPKC and F-actin dynamics promote Hippo pathway polarity in asymmetrically dividing neuroblasts.

Overview

Authors: Niranjan S. Joshi1, Victoria M. Sullivan1, Sherzod A. Tokamov2,3, Richard G. Fehon2,3
  1. The College, The University of Chicago, Chicago, IL 60637, USA
  2. Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, IL 60637, USA
  3. Committee on Development, Regeneration, and Stem Cell Biology, The University of Chicago, Chicago, IL 60637, USA
Institutions: University of Chicago (United States)
Journal: Biology open, volume 15, issue 3, article bio062356
Dates: received 4 November 2025; accepted 28 January 2026; published online 9 March 2026; in print March 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1242/bio.062356 · PMID 41641588 · PMCID PMC13035065 · OpenAlex W7127913829
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: drosophila (organism), cellular / molecular (subfield)
Methods: Statistics
Keywords: Kibra, aPKC, Hippo, Mitosis, Polarity, Cytoskeleton
MeSH: Actins*, Asymmetric Cell Division*, Cell Polarity*, Drosophila Proteins*, Intracellular Signaling Peptides and Proteins*, Neural Stem Cells*, Protein Kinase C*, Protein Serine-Threonine Kinases*, Signal Transduction*, Animals, Drosophila melanogaster, Hippo Kinases, Hippo Signaling Pathway, Tumor Suppressor Proteins (* major topic)
Topic: Hippo pathway signaling and YAP/TAZ (Cell Biology, Biochemistry, Genetics and Molecular Biology), according to OpenAlex
Funding: University of Chicago; NIGMS (GM007183); NSF; NIH (R01NS034783)
Citations: cited by 1 paper (Europe PMC); 45 references in the paper

Abstract

The Hippo signaling pathway is conventionally known to restrict tissue growth in animals. Genetic studies have also shown that loss of Hippo pathway components leads to defects in asymmetric cell division in Drosophila neural stem cells, known as neuroblasts. The hallmark of neuroblast division is the asymmetric localization of aPKC/Bazooka (Par-3)/Par-6 complex, termed the Par complex, to the apical cell cortex. However, the localization of the Hippo pathway components in neuroblasts remains unknown. Here, we report that two key activators of the Hippo pathway, Kibra and Salvador, polarize to the apical cortex of mitotic neuroblasts. We show that apical polarity, via the activity of aPKC, and F-actin dynamics synergize to drive Kibra polarization. Together, these results provide further insights into the relationship between apical polarity and Hippo pathway organization and suggest a possible mechanism by which pathway activity is regulated during neuroblast asymmetric division.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

The paper links to its data, not to its authors' code: see the Data section.

Tracing map

A tracing map links a paper to the code its authors published: this paper has none, so it has no map.

Data

Datasets cited

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 4 authors, 6 keywords, 14 MeSH terms, 4 funders, 45 references.

Cite

This paper

Joshi, N. S., Sullivan, V. M., Tokamov, S. A., & Fehon, R. G. (2026). aPKC and F-actin dynamics promote Hippo pathway polarity in asymmetrically dividing neuroblasts. Biology open, 15(3), bio062356. https://doi.org/10.1242/bio.062356

BibTeX

@article{joshi2026apkc,
author = {Joshi, Niranjan S. and Sullivan, Victoria M. and Tokamov, Sherzod A. and Fehon, Richard G.},
title = {{aPKC and F-actin dynamics promote Hippo pathway polarity in asymmetrically dividing neuroblasts}},
journal = {Biology open},
year = {2026},
month = mar,
volume = {15},
number = {3},
pages = {bio062356},
publisher = {Company of Biologists},
issn = {2046-6390},
doi = {10.1242/bio.062356},
url = {https://doi.org/10.1242/bio.062356},
pmid = {41641588},
pmcid = {PMC13035065}
}

RIS

TY - JOUR
AU - Joshi, Niranjan S.
AU - Sullivan, Victoria M.
AU - Tokamov, Sherzod A.
AU - Fehon, Richard G.
TI - aPKC and F-actin dynamics promote Hippo pathway polarity in asymmetrically dividing neuroblasts
T2 - Biology open
J2 - Biol Open
PY - 2026
DA - 2026/03/09
VL - 15
IS - 3
SP - bio062356
SN - 2046-6390
PB - Company of Biologists
DO - 10.1242/bio.062356
UR - https://doi.org/10.1242/bio.062356
LA - en
ER -

CSL-JSON

{
"id": "10.1242/bio.062356",
"type": "article-journal",
"title": "aPKC and F-actin dynamics promote Hippo pathway polarity in asymmetrically dividing neuroblasts",
"container-title": "Biology open",
"author": [
{
"family": "Joshi",
"given": "Niranjan S."
},
{
"family": "Sullivan",
"given": "Victoria M."
},
{
"family": "Tokamov",
"given": "Sherzod A."
},
{
"family": "Fehon",
"given": "Richard G."
}
],
"container-title-short": "Biol Open",
"volume": "15",
"issue": "3",
"page": "bio062356",
"DOI": "10.1242/bio.062356",
"PMID": "41641588",
"PMCID": "PMC13035065",
"ISSN": "2046-6390",
"publisher": "Company of Biologists",
"URL": "https://doi.org/10.1242/bio.062356",
"language": "en",
"issued": {
"date-parts": [
[
2026,
3,
9
]
]
}
}

Similar papers

The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.

[1] doi:10.1371/journal.pgen.1012260
Hippo signaling regulates cuticle pigmentation and dopamine metabolism in Drosophila.
Journal: PLoS genetics
In common: drosophila, cellular / molecular, 3 references
[2] doi:10.1038/s41556-026-01965-1 [code]
Long-range mutual activation establishes Rho and Rac polarity during cell migration.
Journal: Nature cell biology
In common: cellular / molecular, 2 references
[3] doi:10.1016/j.cub.2026.07.041 [code]
Notch-mediated lateral inhibition is shaped by morphological differences to reinforce bias toward signal-sending or -receiving roles.
Journal: Current biology : CB
In common: drosophila, cellular / molecular, 1 reference
[4] doi:10.1016/j.celrep.2026.117680 [code]
Orb2 RNA-binding activity promotes neural stem cell development and brain growth in Drosophila larvae.
Journal: Cell reports
In common: drosophila, 1 reference
[5] doi:10.1080/15476286.2026.2682069
The RNA-binding activity of the <i>Drosophila</i> Brat protein is necessary for viability and mRNA regulation.
Journal: RNA biology
In common: drosophila, 1 reference
[6] doi:10.1126/sciadv.aed8818 [code]
Reconstitution of actomyosin networks in cell-sized liposomes dissects distinct mechanisms of membrane blebbing and symmetry breaking.
Journal: Science advances
In common: cellular / molecular, 1 reference
[7] doi:10.1038/s44318-026-00724-0
Microcephaly-associated protein WDR62 supports purine metabolism by interacting with co-chaperone BAG2.
Journal: The EMBO journal
In common: cellular / molecular, 1 reference
[8] doi:10.1038/s41598-026-41460-z [code]
NvashA function reveals temporal differences in neural subtype generation in cnidarians.
Journal: Scientific reports
In common: 1 reference
[9] doi:10.1371/journal.pbio.3003959 [code]
Recurrent synapses between CO2-sensitive olfactory sensory neurons enable robust CO2 detection in Aedes aegypti mosquitoes.
Journal: PLoS biology
In common: drosophila, cellular / molecular
[10] doi:10.1073/pnas.2619143123
Cell-type-specific circadian and light-responsive transcriptional dynamics in adult <i>Drosophila</i> neurons.
Journal: Proceedings of the National Academy of Sciences of the United States of America
In common: drosophila, cellular / molecular

Contribute

The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.

Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.

Request its removal

To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).

Discussion, reproductions, activity

Discussion: questions and error reports about this paper and its code, from signed-in readers and its authors. It opens with sign-in.

Reproductions: reports from readers who ran the authors' code: what they reproduced, with which environment, commit and data. It opens with sign-in.

Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.