A new member of the spalt like zinc finger protein family, Msal-3, is expressed in the CNS and sites of epithelial/mesenchymal interaction

Ott, Thomas; Parrish, Mark E.; Bond, Kristin; Schwaeger-Nickolenko, Anja; Monaghan, A. Paula

doi:10.1016/s0925-4773(00)00552-9

Cited by 41 publications

(63 citation statements)

References 8 publications

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“…This raises the possibility that neurons are differentiating prematurely. To ensure that the cells in the PP and CP were not misplaced PCs, the expression of the VZ PC markers Nestin, Pax-6, Sall1, Sall3, and the SVZ marker SVET (subventricular tag) (Ott et al, 1996(Ott et al, , 2001Chapouton et al, 1999;Tarabykin et al, 2001;Anderson et al, 2002) was compared by in situ hybridization throughout the dorsal telencephalon from E10.0 until E16.5. No differences in the regional expression of the VZ or SVZ PC markers were observed between wild-type and mutant animals, indicating that the VZ and SVZ are molecularly distinct and confined to the ventricular surface (data not shown).…”

Section: Neurons Differentiate Prematurely In Tlxmentioning

confidence: 99%

TheTlxGene Regulates the Timing of Neurogenesis in the Cortex

Roy¹,

Kuznicki²,

Wu³

et al. 2004

J. Neurosci.

134

139

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The tailless (tlx) gene is a forebrain-restricted transcription factor. Tlx mutant animals exhibit a reduction in the size of the cerebral hemispheres and associated structures (Monaghan et al., 1997). Superficial cortical layers are specifically reduced, whereas deep layers are relatively unaltered (Land and Monaghan, 2003). To determine whether the adult laminar phenotype has a developmental etiology and whether it is associated with a change in proliferation/differentiation decisions, we examined the cell cycle and neurogenesis in the embryonic cortex. We found that there is a temporal and regional requirement for the Tlx protein in progenitor cells (PCs). Neurons prematurely differentiate at all rostrocaudal levels up to mid-neurogenesis in mutant animals. Heterozygote animals have an intermediate phenotype indicating there is a threshold requirement for Tlx in early cortical neurogenesis. Our studies indicate that PCs in the ventricular zone are sensitive to loss of Tlx in caudal regions only; however, PCs in the subventricular zone are altered at all rostrocaudal levels in tlx-deficient animals. Furthermore, we found that the cell cycle is shorter from embryonic day 9.5 in tlx Ϫ/Ϫ embryos. At mid-neurogenesis, the PC population becomes depleted, and late PCs have a longer cell cycle in tlx-deficient animals. Consequently, later generated structures, such as upper cortical layers, the dentate gyrus, and the olfactory bulbs, are severely reduced. These studies indicate that tlx is an essential intrinsic regulator in the decision to proliferate or differentiate in the developing forebrain.

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Section: Neurons Differentiate Prematurely In Tlxmentioning

confidence: 99%

TheTlxGene Regulates the Timing of Neurogenesis in the Cortex

Roy¹,

Kuznicki²,

Wu³

et al. 2004

J. Neurosci.

134

139

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“…The four orthologues vertebrate proteins, Sall1-4, display differences in the finger distribution, being Sall2 the more distant member of the family ( Fig. 1; Kohlhase et al, 1996;Hollemann et al, 1996;Kohlhase et al, 1999a;Onuma et al, 1999;Ott et al, 1996;Buck et al, 2000;Ott et al, 2001;Ma et al, 2001;Kohlhase et al, 2002a;Ma et al, 2006). The nematode Sall protein, named Sem-4, shares common features with their homologues, like the finger domains 3 and 5 ( Fig.…”

mentioning

confidence: 99%

Regulation and function of Spalt proteins during animal development

Celis¹,

Barrio²

2009

Int. J. Dev. Biol.

122

124

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The genes of the spalt (sal) family play fundamental roles during animal development. The two members of this family in Drosophila, spalt (sal) and spalt-related (salr) encode Znfinger transcription factors that link the Decapentaplegic (Dpp)/BMP signalling pathway to the patterning of the wing. They are regulated by the Dpp pathway in the wing disc, and they were shown to mediate some of the morphogenetic activities of the Dpp/BMP4 secreted ligand. The sal genes were initially found by virtue of mutations that produce homeotic transformations in the head and tail of the Drosophila embryo. Since then, a number of other requirements have been associated to these genes in Drosophila, including morphogenesis of the respiratory system, cell fate specification of sensory organs and the differentiation of several photoreceptor cells, among others. Vertebrate sal orthologues (spalt-like/sall) have also important developmental roles during neural development and organogenesis, and at least two human sall genes are linked to the genetic diseases Townes Brocks Syndrome (TBS; SALL1 ) and Okihiro Syndrome (OS; SALL4). In this review, we will summarize the main characteristics of the sall genes and proteins, pointing out to the similarities in their developmental roles during Drosophila and vertebrate development.

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“…It plays an important role in terminal differentiation of photoreceptors, tracheal development, 5 and wing vein placement. 6 Sal-related genes have been isolated from Caenorhabditis elegans, 7 fish, 8,9 Xenopus, 10,11 mice, 12,13 and humans. 14 Each of these homologs is expressed during embryonic development and in specific adult tissues.…”

mentioning

confidence: 99%

Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia

Cui

Kong

Ma³

et al. 2006

Modern Pathology

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CanadaSALL4, a newly identified zinc-finger transcriptional factor important for embryonic development, is mapped to chromosome 20q13. Previously, we reported that SALL4 was constitutively expressed in acute myeloid leukemia and SALL4 transgenic mice developed acute myeloid leukemia. In this study, we aimed to survey SALL4 protein expression in benign and neoplastic hematopoietic tissues in addition to acute myeloid leukemia using immunostaining with a polyclonal anti-SALL4 antibody. Primary hematological tumors (178) and 15 benign hematopoietic tissues were examined. Reverse transcription-polymerase chain reaction was also performed to detect SALL4 mRNA expression on eight precursor B-cell lymphoblastic leukemia/lymphomas, 10 benign hematopoietic tissues, and seven hematopoietic cancer cell lines. Of the benign tissues, SALL4 expression was detectable only in CD34 þ hematopoietic stem/progenitor cells (2/2 at protein level, 3/3 at RNA level). In neoplastic tissues, only precursor B-cell lymphoblastic leukemia/lymphomas had detectable SALL4 (12/16 at protein level, 7/8 at RNA level), similar to that observed in acute myeloid leukemia. Of the seven cell lines examined, only those derived from acute myeloid leukemia and precursor B-cell lymphoblastic leukemia/ lymphomas were positive. To conclude, SALL4 expression is normally restricted to CD34 þ hematopoietic stem/ progenitor cells. The persistence of SALL4 expression in leukemic blasts in precursor B-cell lymphoblastic leukemia/lymphomas resembles to what we observed in acute myeloid leukemia, and correlates with the maturation arrest of these cells. We have shown in our previous study that the constitutive expression of SALL4 in mice can lead to acute myeloid leukemia development. The similar expression pattern of SALL4 in acute myeloid leukemia and B-cell lymphoblastic leukemia/lymphomas suggests that these two disease entities may share similar biological features and/or mechanisms of leukemogenesis. More definite studies to investigate the role of SALL4 in the pathogenesis of B-cell lymphoblastic leukemia/lymphomas are needed in the future to address this question.

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A new member of the spalt like zinc finger protein family, Msal-3, is expressed in the CNS and sites of epithelial/mesenchymal interaction

Cited by 41 publications

References 8 publications

TheTlxGene Regulates the Timing of Neurogenesis in the Cortex

TheTlxGene Regulates the Timing of Neurogenesis in the Cortex

Regulation and function of Spalt proteins during animal development

Differential expression of the novel oncogene, SALL4, in lymphoma, plasma cell myeloma, and acute lymphoblastic leukemia

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