Expression of the zinc finger gene fez-like in zebrafish forebrain

Hashimoto, Hisashi; Yabe, Taijiro; Hirata, Tsutomu; Shimizu, Takashi; Bae, Young-Ki; Yamanaka, Yojiro; Hirano, Toshio; Hibi, Masahiko

doi:10.1016/s0925-4773(00)00418-4

Cited by 70 publications

(89 citation statements)

References 22 publications

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“…5A, available at www.jneurosci.org as supplemental material), which could represent another splice variant. This sized PINK1 band has been described in the human brain Consistent with loss of PINK1 causing increased GSK3␤ activity, we observed an increase in the expression of fezl (a gene regulated by the wnt/GSK3␤ pathway) (Hashimoto et al, 2000b) and its downstream target neurogenin-1 in our PINK1 morphants. Our PINK1 morphants had decreased numbers of dopaminergic neurons, whereas neurogenin-1 overexpression in otherwise normal zebrafish leads to an increase in this neuronal population (Jeong et al, 2006).…”

Section: Discussionsupporting

confidence: 89%

Loss of PINK1 Function Affects Development and Results in Neurodegeneration in Zebrafish

Anichtchik

Diekmann²,

Fleming³

et al. 2008

J. Neurosci.

155

115

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Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder in the Western world. PTEN (phosphatase/tensin homolog on chromosome 10)-induced putative kinase 1 (PINK1), a putative kinase that is mutated in autosomal recessive forms of PD, is also implicated in sporadic cases of the disease. Although the mutations appear to result in a loss of function, the roles of this protein and the pathways involved in PINK1 PD are poorly understood. Here, we generated a vertebrate model of PINK1 insufficiency using morpholino oligonucleotide knockdown in zebrafish (Danio rerio). PINK1 knockdown results in a severe developmental phenotype that is rescued by wild-type human PINK1 mRNA. Morphants display a moderate decrease in the numbers of central dopaminergic neurons and alterations of mitochondrial function, including increases in caspase-3 activity and reactive oxygen species (ROS) levels. When the morphants were exposed to several drugs with antioxidant properties, ROS levels were normalized and the associated phenotype improved. In addition, GSK3␤-related mechanisms can account for some of the effects of PINK1 knockdown, as morphant fish show elevated GSK3␤ activity and their phenotype is partially abrogated by GSK3␤ inhibitors, such as LiCl and SB216763 [3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)1H-pyrrole-2,5-dione]. This provides new insights into the biology of PINK1 and a possible therapeutic avenue for further investigation.

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Section: Discussionsupporting

confidence: 89%

Loss of PINK1 Function Affects Development and Results in Neurodegeneration in Zebrafish

Anichtchik

Diekmann²,

Fleming³

et al. 2008

J. Neurosci.

155

115

View full text Add to dashboard Cite

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“…The highest expression ratio among the transcription factors was 9.7 for the zinc finger protein 312 (also known as forebrain embryonic zinc finger, Fez). Zinc finger protein 312/Fez contains six C2H2-type zinc finger domains and is highly conserved in diverse species (Hashimoto et al, 2000;Matsuo-Takasaki et al, 2000;Yang et al, 2001;Levkowitz et al, 2003). Figure 4C shows that zinc finger protein 312 is robustly expressed in the SON and cortex (see also MatsuoTakasaki et al, 2000) and increases more than twofold during hyperosmolar conditions (Table 3).…”

Section: Discussionmentioning

confidence: 88%

Selective Gene Expression in Magnocellular Neurons in Rat Supraoptic Nucleus

Mutsuga¹,

Shahar²,

Verbalis³

et al. 2004

J. Neurosci.

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Oxytocin-and vasopressin-producing magnocellular neurons (MCNs) of the hypothalamo-neurohypophysial system are the only neuronal phenotypes present in the rat supraoptic nucleus (SON). Laser microdissection of the SON, extraction and T7-based amplification of its RNAs, and analysis of the resulting cDNAs by hybridization on a 35, 319 element DNA microarray have provided a detailed composite view of the gene expression profile of the MCNs. The genes expressed in the SON were compared with those expressed in a reference tissue consisting of total hypothalamus, and this "expression ratio" indicated which genes were preferentially expressed in the SON. Of the 26,000 unique genes on the array, 1385 were found to be expressed in the SON at levels more than two times greater than in the hypothalamus as a whole. Of these, 123 were expressed Ն3.4-fold higher in the SON versus hypothalamus. Most of these preferentially expressed genes were not previously known to be expressed in the MCNs. Quantitative and double-label in situ hybridization histochemistry was used selectively to confirm a number of these microarray observations and to evaluate the osmotic regulation and cell-specific expression of these genes, respectively.

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“…The Fezl ORF encodes a protein of 455 amino acids that contains six C 2 H 2 -type zinc-finger motifs and an eh1 domain, which is conserved in several transcriptional repressors (12,14). To generate Fezl-deficient mice, we replaced the entire Fezl ORF with a promoterless EGFP-IRES-PLAP (EGFP, enhanced GFP; IRES, internal ribosomal entry site) cassette (18).…”

Section: Resultsmentioning

confidence: 99%

“…Interestingly, the recruitment of Groucho corepressors is mediated by the engrailed homology (eh1) domains of homeodomain proteins (27). Fezl also contains an eh1 motif (12), raising the possibility that Groucho family members may interact with Fezl to regulate differentiation in the developing cortex. However, our data suggest that Fezl does not actively suppress the acquisition of alternative laminar identities during cortical development, because we saw no expansion of markers for upper layer neurons into the deep layers, nor did we detect an expansion of markers for layers 5 or 6 (apart from Igfbp4) into inappropriate layers.…”

Section: Discussionmentioning

confidence: 99%

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Fezl regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex

Chen

Schaevitz

McConnell

2005

Proc. Natl. Acad. Sci. U.S.A.

333

400

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During the development of the cerebral cortex, progenitor cells produce neurons that migrate to laminar positions appropriate for their birth dates, adopt specific neuronal identities, and form appropriate local and long-distance axonal connections. Here, we report that forebrain embryonic zinc-finger-like protein (Fezl), a putative zinc-finger transcriptional repressor, is required for the differentiation of projection neurons in cortical layer 5. In Fezldeficient mice, these neurons display molecular, morphological, and axonal targeting defects. The corticospinal tract was absent in Fezl ؊/؊ mice, corticotectal and pontine projections were severely reduced, and Fezl-expressing neurons formed aberrant axonal projections. The expression of many molecular markers for deeplayer neurons was reduced or absent in the Fezl ؊/؊ cerebral cortex. Most strikingly, Ctip2, a transcription factor required for the formation of the corticospinal tract, was not expressed in the Fezl-deficient cortex. These results suggest that Fezl regulates the differentiation of layer 5 subcortical projection neurons.axon guidance ͉ cell fate ͉ corticospinal tract ͉ zinc-finger transcription factor

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Expression of the zinc finger gene fez-like in zebrafish forebrain

Cited by 70 publications

References 22 publications

Loss of PINK1 Function Affects Development and Results in Neurodegeneration in Zebrafish

Loss of PINK1 Function Affects Development and Results in Neurodegeneration in Zebrafish

Selective Gene Expression in Magnocellular Neurons in Rat Supraoptic Nucleus

Fezl regulates the differentiation and axon targeting of layer 5 subcortical projection neurons in cerebral cortex

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