KIF14 controls ciliogenesis via regulation of Aurora A and is important for Hedgehog signaling

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F20%3A00114130" target="_blank" >RIV/00216224:14110/20:00114130 - isvavai.cz</a>

Výsledek na webu

<a href="https://rupress.org/jcb/article/219/6/e201904107/151721/KIF14-controls-ciliogenesis-via-regulation-of?searchresult=1" target="_blank" >https://rupress.org/jcb/article/219/6/e201904107/151721/KIF14-controls-ciliogenesis-via-regulation-of?searchresult=1</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1083/jcb.201904107" target="_blank" >10.1083/jcb.201904107</a>

Jazyk výsledku

angličtina

Název v původním jazyce

KIF14 controls ciliogenesis via regulation of Aurora A and is important for Hedgehog signaling

Popis výsledku v původním jazyce

Primary cilia play critical roles in development and disease. Their assembly and disassembly are tightly coupled to cell cycle progression. Here, we present data identifying KIF14 as a regulator of cilia formation and Hedgehog (HH) signaling. We show that RNAi depletion of KIF14 specifically leads to defects in ciliogenesis and basal body (BB) biogenesis, as its absence hampers the efficiency of primary cilium formation and the dynamics of primary cilium elongation, and disrupts the localization of the distal appendage proteins SCLT1 and FBF1 and components of the IFT-B complex. We identify deregulated Aurora A activity as a mechanism contributing to the primary cilium and BB formation defects seen after KIF14 depletion. In addition, we show that primary cilia in KIF14-depleted cells are defective in response to HH pathway activation, independently of the effects of Aurora A. In sum, our data point to KIF14 as a critical node connecting cell cycle machinery, effective ciliogenesis, and HH signaling.

Název v anglickém jazyce

KIF14 controls ciliogenesis via regulation of Aurora A and is important for Hedgehog signaling

Popis výsledku anglicky

Primary cilia play critical roles in development and disease. Their assembly and disassembly are tightly coupled to cell cycle progression. Here, we present data identifying KIF14 as a regulator of cilia formation and Hedgehog (HH) signaling. We show that RNAi depletion of KIF14 specifically leads to defects in ciliogenesis and basal body (BB) biogenesis, as its absence hampers the efficiency of primary cilium formation and the dynamics of primary cilium elongation, and disrupts the localization of the distal appendage proteins SCLT1 and FBF1 and components of the IFT-B complex. We identify deregulated Aurora A activity as a mechanism contributing to the primary cilium and BB formation defects seen after KIF14 depletion. In addition, we show that primary cilia in KIF14-depleted cells are defective in response to HH pathway activation, independently of the effects of Aurora A. In sum, our data point to KIF14 as a critical node connecting cell cycle machinery, effective ciliogenesis, and HH signaling.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10601 - Cell biology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2020

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

JOURNAL OF CELL BIOLOGY

ISSN

0021-9525

e-ISSN

1540-8140

Svazek periodika

219

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

29

Strana od-do

„1-23“-„S1-S6“

Kód UT WoS článku

000538141100021

EID výsledku v databázi Scopus

2-s2.0-85084170141