Sequence and embryonic expression of three zebrafish fringe genes: lunatic fringe, radical fringe, and manic fringe

Qiu, Xuehui; Xu, Haoying; Haddon, Catherine; Lewis, Julian; Jiang, Yun-Jin

doi:10.1002/dvdy.20155

Cited by 33 publications

(30 citation statements)

References 62 publications

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“…Single WISH was done as described previously (Qiu et al, 2004). For immunohistochemical staining, embryos were anesthetized, dechorinated and fixed in 4% paraformaldehyde (PFA)/phosphate-buffered saline (PBS) at 4°C, unless otherwise stated.…”

Section: Whole-mount Mrna In Situ Hybridization (Wish) and Immunohistmentioning

confidence: 99%

Udu Deficiency Activates DNA Damage Checkpoint

Lim

Chong

Jiang

2009

MBoC

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Udu has been shown to play an essential role during blood cell development; however, its roles in other cellular processes remain largely unexplored. In addition, ugly duckling (udu) mutants exhibited somite and myotome boundary defects. Our fluorescence-activated cell sorting analysis also showed that the loss of udu function resulted in defective cell cycle progression and comet assay indicated the presence of increased DNA damage in udu tu24 mutants. We further showed that the extensive p53-dependent apoptosis in udu tu24 mutants is a consequence of activation in the Atm-Chk2 pathway. Udu seems not to be required for DNA repair, because both wild-type and udu embryos similarly respond to and recover from UV treatment. Yeast two-hybrid and coimmunoprecipitation data demonstrated that PAH-L repeats and SANT-L domain of Udu interacts with MCM3 and MCM4. Furthermore, Udu is colocalized with 5-bromo-2 -deoxyuridine and heterochromatin during DNA replication, suggesting a role in maintaining genome integrity. INTRODUCTIONugly duckling (udu tu24 ) mutant was first isolated from the 1996 Tü bingen screen and has been shown to exhibit a short body-axis with massive cell death (Hammerschmidt et al., 1996). Another udu allele, udu sq1 , was isolated in a genetic screen aiming at mutants with defects in hematopoiesis (Liu et al., 2007). Positional cloning revealed that Udu protein encodes a novel nuclear factor consisting of three conserved regions (CR-1, CR-2, and CR-3) that do not share similarity with any known domains, two paired amphipathic ␣-helix like (PAH-L) repeats, and one putative SW13, ADA2, N-Cor and TFIIIB like (SANT-L) domain. The C-terminal PAH-L and SANT-L domains have been shown to be essential in primitive erythroid cell development (Liu et al., 2007). The PAH domain, first identified in yeast SIN3 (Wang et al., 1990), has been demonstrated to mediate protein-protein interactions (Spronk et al., 2000). SIN3 has no intrinsic DNA binding ability and has to be targeted to gene promoters by interacting with DNA binding proteins, thereafter positively and negatively regulating genes involved in diverse cellular functions (Silverstein and Ekwall, 2005). The SANT domain is a highly conserved motif with similarity to Myb DNA binding domain (Aasland et al., 1996), which has been shown to be critical in regulating chromatin accessibility (Boyer et al., 2002(Boyer et al., , 2004.The DNA damage response pathway is a cellular surveillance system that senses the presence of damaged DNA and elicits checkpoint activation and subsequent lesion repair in preventing amplification or loss of genes or chromosomes (Zhou and Elledge, 2000). The critical components of DNA damage checkpoint are two phosphatidyl inositol 3-kinaselike kinase family proteins: Ataxia telangiectasia mutated (ATM) and ATM-and Rad3-related (ATR) (Abraham, 2003;Shiloh, 2003). ATR functions as a sensor and transducer in response to UV light and presumably to genotoxic agents that give rise to stalled replication forks, and subsequently activates Checkp...

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Section: Whole-mount Mrna In Situ Hybridization (Wish) and Immunohistmentioning

confidence: 99%

Udu Deficiency Activates DNA Damage Checkpoint

Lim

Chong

Jiang

2009

MBoC

Self Cite

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“…The segments in the three shades of gray indicate an absence of the relevant loss-of-function data. References: a (Bierkamp and Campos-Ortega, 1993), b (van Eeden et al, 1996, d (Holley et al, 2002), e (Westin and Lardelli, 1997), f , g (Dornseifer et al, 1997), h , i , j , k (Jü lich et al, 2005b), l (Prince et al, 2001), m (Qiu et al, 2004), n (Topczewska et al, 2003), o (Ishitani et al, 2005), p (Jiang et al, 1996), q (Itoh et al, 2003), r , and s (Echeverri and Oates, 2007 There is evidence that Delta can also cell-autonomously inhibit the ability of a cell to receive a Delta signal from an adjacent cell (Bray, 2006). The mouse Deltalike-3, which is required for murine segmentation, appears to specifically function in this inhibitory manner (Ladi et al, 2005).…”

Section: The Notch Pathway and Zebrafish Segmentationmentioning

confidence: 99%

The genetics and embryology of zebrafish metamerism

Holley

2007

Developmental Dynamics

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123

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“…By combining pet1 in situ hybridization with the detection of rfng transcripts to identify rhombomeric borders (Qiu et al, 2004), we observed that the first pet1-positive cells were located in r1, close to the MHB (data not shown). Because previous results from our laboratory also suggested that the MHB progenitor pool contributed neurons to the ventral anterior hindbrain (Tallafuss and Bally-Cuif, 2003), we specifically tested for the contribution of this pool to r1-2 serotonergic precursors.…”

Section: Pet1-positive Cells Located In R1-2 Originate From the Midbrmentioning

confidence: 99%

“…The following probes were used: tph2 (previously tphR; Teraoka et al, 2004), tph1 (previously tphD1; Bellipanni et al, 2002), and radical fringe (rfng; Qiu et al, 2004). The RZPD EST clone IMAGp998C2214692Q was used to detect pet1 transcripts.…”

Section: In Situ Hybridization and Immunohistochemistrymentioning

confidence: 99%

The serotonergic phenotype is acquired by converging genetic mechanisms within the zebrafish central nervous system

Lillesaar¹,

Tannhäuser²,

Stigloher³

et al. 2007

Developmental Dynamics

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To gain knowledge about the developmental origin of serotonergic precursors and the regulatory cascades of serotonergic differentiation in vertebrates, we determined the spatiotemporal expression profile of the Ets-domain transcription factor-encoding gene pet1 in developing and adult zebrafish. We show that it is an early, specific marker of raphe serotonergic neurons, but not of other serotonergic populations. We then use pet1 expression together with tracing techniques to demonstrate that serotonergic neurons of rhombomeres (r) 1-2 largely originate from a progenitor pool at the midbrain-hindbrain boundary. Furthermore, by combining expression analyses of pet1 and the raphe tryptophan hydroxylase (Tph2) with rhombomere identity markers, we show that anterior and posterior hindbrain clusters of serotonergic precursors are separated by r3, rather than r4 as in other vertebrates. Our findings establish the origin of r1-2 serotonergic precursors, and strengthen the evidence for molecular, ontogenic and phylogenic heterogeneities among the vertebrate brain serotonergic cell populations. Developmental Dynamics 236: 1072-1084, 2007.

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Sequence and embryonic expression of three zebrafish fringe genes: lunatic fringe, radical fringe, and manic fringe

Cited by 33 publications

References 62 publications

Udu Deficiency Activates DNA Damage Checkpoint

Udu Deficiency Activates DNA Damage Checkpoint

The genetics and embryology of zebrafish metamerism

The serotonergic phenotype is acquired by converging genetic mechanisms within the zebrafish central nervous system

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