PUBLICATION

Regulation of neurocoel morphogenesis by Pard6gammab

Authors

Munson, C., Huisken, J., Bit-Avragim, N., Kuo, T., Dong, P.D., Ober, E.A., Verkade, H., Abdelilah-Seyfried, S., and Stainier, D.Y.

ID

ZDB-PUB-081001-10

Date

2008

Source

Developmental Biology 324(1): 41-54 (Journal)

Registered Authors

Abdelilah-Seyfried, Salim, Dong, P. Duc, Ober, Elke, Stainier, Didier, Verkade, Heather

Keywords

Par6, neurulation, apicobasal polarity, epithelium, zebrafish

MeSH Terms

Zebrafish Proteins/genetics
Zebrafish Proteins/physiology*
Epithelium/embryology
Morphogenesis
Mutation
Adaptor Proteins, Signal Transducing/genetics
Adaptor Proteins, Signal Transducing/physiology*
Zebrafish/embryology*
Zebrafish/physiology
Cell Polarity
Neural Tube/embryology*
Neural Tube/physiology
Spindle Apparatus/physiology
Animals
Neurulation

(all 15)

PubMed

18817769 Full text @ Dev. Biol.

Abstract

The Par3/Par6/aPKC protein complex plays a key role in the establishment and maintenance of apicobasal polarity, a cellular characteristic essential for tissue and organ morphogenesis, differentiation and homeostasis. During a forward genetic screen for liver and pancreas mutants, we identified a pard6gammab mutant, representing the first known pard6 mutant in a vertebrate organism. pard6gammab mutants exhibit defects in epithelial tissue development as well as multiple lumens in the neural tube. Analyses of the cells lining the neural tube cavity, or neurocoel, in wildtype and pard6gammab mutant embryos show that lack of Pard6gammab function leads to defects in mitotic spindle orientation during neurulation. We also found that the PB1 (aPKC-binding) and CRIB (Cdc-42-binding) domains and the KPLG amino acid sequence within the PDZ domain (Pals1-and Crumbs binding) are not required for Pard6gammab localization but are essential for its function in neurocoel morphogenesis. Apical membranes are reduced, but not completely absent, in mutants lacking the zygotic, or both the maternal and zygotic, function of pard6gammab, leading us to examine the localization and function of the three additional zebrafish Pard6 proteins. We found that Pard6alpha, but not Pard6beta or Pard6gammaa, could partially rescue the pard6gammab(s441) mutant phenotypes. Altogether, these data indicate a previously unappreciated functional diversity and complexity within the vertebrate pard6 gene family.

Genes / Markers

Figures

Show all Figures

Expression

Gene	Antibody	Fish	Conditions	Stage	Anatomy	Assay	Figure
myl7		pard6gb^s441/s441	standard conditions	Prim-15	heart tube	ISH	Fig. 1
myl7		pard6gb^s441/s441	standard conditions	Prim-5	neural tube epithelial cell	ISH	Fig. 2
myl7		WT	standard conditions	Prim-15	heart tube	ISH	Fig. 1
myl7		WT	standard conditions	Prim-5	neural tube epithelial cell	ISH	Fig. 2
pals1a	Ab3-pals1a	pard6gb^s441/s441	standard conditions	Prim-5	neural tube epithelial cell	IHC	Fig. 2
pals1a	Ab3-pals1a	WT	standard conditions	Prim-5	neural tube epithelial cell	IHC	Fig. 2
pard6b		WT	standard conditions	14-19 somites to 26+ somites	otic placode	ISH	Fig. S4
pard6gb		WT	standard conditions	14-19 somites	neural tube	ISH	Fig. 3
pard6gb		WT	standard conditions	Prim-5	neural tube	ISH	Fig. 3
pard6gb		WT	standard conditions	Bud	whole organism	ISH	Fig. 3

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Phenotype

Fish	Conditions	Stage	Phenotype	Figure
WT + MO1-pard6gb	standard conditions	Prim-25	central canal malformed, abnormal	Fig. 3
WT + MO1-pard6gb	standard conditions	Prim-25	embryonic heart tube development disrupted, abnormal	Fig. 3
WT + MO1-pard6gb	standard conditions	Prim-25	ventricular system collapsed, abnormal	Fig. 3
WT + MO1-pard6gb	standard conditions	Prim-25	whole organism curved dorsal, abnormal	Fig. 3
pals1a^m520/m520	standard conditions	Prim-5	central canal malformed, abnormal	Fig. 7
pals1a^m520/m520	standard conditions	Prim-5	neural tube formation disrupted, abnormal	Fig. 7
pals1a^m520/m520	standard conditions	Prim-5	neural tube malformed, abnormal	Fig. 7
pals1a^m520/m520; pard6gb^s441/s441	standard conditions	Prim-5	central canal malformed, abnormal	Fig. 7
pals1a^m520/m520; pard6gb^s441/s441	standard conditions	Prim-5	neural tube formation disrupted, abnormal	Fig. 7
pals1a^m520/m520; pard6gb^s441/s441	standard conditions	Prim-5	neural tube malformed, abnormal	Fig. 7

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Mutations / Transgenics

Allele	Construct	Type	Affected Genomic Region
m520		Point Mutation	pals1a
m567		Point Mutation	prkci
s441		Point Mutation	pard6gb
s854Tg	Tg(Xla.Eef1a1:GFP)	Transgenic Insertion

Human Disease / Model

Sequence Targeting Reagents

Target	Reagent	Reagent Type
pard6a	MO1-pard6a	MRPHLNO
pard6gb	MO1-pard6gb	MRPHLNO

Fish

Fish
pals1a^m520/m520
pals1a^m520/m520; pard6gb^s441/s441
pard6gb^s441/s441
pard6gb^s441/s441
pard6gb^s441/s441; prkci^m567/m567
s854Tg
WT
WT + MO1-pard6gb

Antibodies

Name	Type	Antigen Genes	Isotypes	Host Organism
Ab1-prkca	polyclonal	prkcaa	IgG	Rabbit
Ab1-tjp1	monoclonal	tjp1a tjp1b	IgG1	Mouse
Ab3-pals1a	polyclonal	pals1a		Rabbit

Orthology

Engineered Foreign Genes

Marker	Marker Type	Name
GFP	EFG	GFP

Mapping

Entity Type	Entity Symbol	Location
GENE	pard6gb	Chr: 19 Details
SSLP	z6079	Chr: 19 Details
SSLP	z9059	Chr: 19 Details

Munson et al., 2008 ZDB-PUB-081001-10 PMID:18817769

Regulation of neurocoel morphogenesis by Pard6gammab

Munson et al., 2008

ZDB-PUB-081001-10
PMID:18817769