GC Box-binding Transcription Factors Control the Neuronal Specific Transcription of the Cyclin-dependent Kinase 5 Regulator p35

Ross, Sarah E.; Tienhaara, Anri; Lee, Ming‐Sum; Tsai, Li‐Huei; Gill, Grace

doi:10.1074/jbc.m110771200

Cited by 45 publications

(63 citation statements)

References 78 publications

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“…7C,D), demonstrating that the p35 promoter is a direct target for HSF2 binding. Furthermore, binding of Sp3 to this region was detected in vivo, which is in agreement with the EMSA analysis performed by Ross et al (2002). Interestingly, impaired binding of Sp3 was consistently observed in E16.5 cortical extracts from Hsf2 −/− mice (Fig.…”

Section: Hsf2 Binds In Vivo To the Proximal Regulatory Region Of The supporting

confidence: 88%

“…To investigate whether HSF2 regulates the p35 gene directly by binding to its promoter, we performed ChIP analysis of CP extracts at E16.5. A 200-base-pair (bp) segment within the p35 promoter is sufficient for p35 expression in rat primary cortical neurons or neurons derived from P19 EC cells (Ross et al 2002). This region, well conserved between mouse and human, contains a putative HSE close to the main transcription initiation site and two GC-boxes (Fig.…”

Section: Hsf2 Binds In Vivo To the Proximal Regulatory Region Of The mentioning

confidence: 99%

“…In addition, p35 −/− mice show more severe defects in the rostral-medial part of the brain, whereas in Hsf2 −/ −mice p35 levels are reduced mainly in the caudo-medial portion of the developing cortex, where the Hsf2 −/− phenotype is most severe in terms of SP disorganization, calretinin expression, and abnormal neuron positioning. The reduction of p35 due to the lack of HSF2 can occur (Ross et al 2002); (arrows) primers used in amplification step of the ChIP assay. The asterisk marks the key nucleotides required for HSF binding (Fujimoto et al 2004).…”

Section: Affected In the Hsf2mentioning

confidence: 99%

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Role of heat-shock factor 2 in cerebral cortex formation and as a regulatorof p35 expression

Chang¹,

Östling²,

Åkerfelt³

et al. 2006

Genes Dev.

109

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Heat-shock factors (HSFs) are associated with multiple developmental processes, but their mechanisms of action in these processes remain largely enigmatic. Hsf2-null mice display gametogenesis defects and brain abnormalities characterized by enlarged ventricles. Here, we show that Hsf2 −/− cerebral cortex displays mispositioning of neurons of superficial layers. HSF2 deficiency resulted in a reduced number of radial glia fibers, the architectural guides for migrating neurons, and of Cajal-Retzius cells, which secrete the positioning signal Reelin. Therefore, we focused on the radial migration signaling pathways. The levels of Reelin and Dab1 tyrosine phosphorylation were reduced, suggesting that the Reelin cascade is affected in Hsf2 −/− cortices. The expression of p35, an activator of cyclin-dependent kinase 5 (Cdk5), essential for radial migration, was dependent on the amount of HSF2 in gain-and loss-of-function systems. p39, another Cdk5 activator, displayed reduced mRNA levels in Hsf2 −/− cortices, which, together with the lowered p35 levels, decreased Cdk5 activity. We demonstrate in vivo binding of HSF2 to the p35 promoter and thereby identify p35 as the first target gene for HSF2 in cortical development. In conclusion, HSF2 affects cellular populations that assist in radial migration and directly regulates the expression of p35, a crucial actor of radial neuronal migration.[Keywords: Corticogenesis; heat-shock factor; p35-Cdk5; radial cortical migration] Supplemental material is available at http://www.genesdev.org. Heat-shock factors (HSFs) were initially discovered to regulate heat-shock genes and the heat-shock response. The heat-shock response, conserved from yeast to man, is characterized by the induction of heat-shock genes encoding molecular chaperones (for review, see Pirkkala et al. 2001). A unique gene constitutes HSF in yeast, nematode, and fruit fly, whereas a family of four members is present in vertebrates. HSF1 and HSF2 are found in all vertebrate species, while HSF3 is specific for avian species and HSF4 is specific for mammals (Rabindran et al. 1991;Sarge et al. 1991;Schuetz et al. 1991;Nakai and Morimoto 1993;Nakai et al. 1997;Råbergh et al. 2000;Hilgarth et al. 2004;Le Goff et al. 2004). In vertebrates, HSF1 is the stress-responsive prototype, which cannot be substituted by any other HSF in stress-inducible hsp gene expression or in acquired thermotolerance (McMillan et al. 1998;Xiao et al. 1999;Zhang et al. 2002).A developmental role for the HSFs began to emerge when the Drosophila HSF was found to be required for oogenesis and early larval development (Jedlicka et al. 1997). Strikingly, these developmental effects of Drosophila HSF are not mediated by hsp gene induction. The basal expression levels of hsps during embryonic development in mouse are not affected by the lack of HSF1 (Xiao et al. 1999). Therefore, other target genes are likely to be controlled by HSF1 in development. Recently, binding of HSF1 and HSF4 to the FGF-7 promoter with opposing effects on FGF-7 gene expression su...

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Section: Hsf2 Binds In Vivo To the Proximal Regulatory Region Of The supporting

confidence: 88%

Section: Hsf2 Binds In Vivo To the Proximal Regulatory Region Of The mentioning

confidence: 99%

Section: Affected In the Hsf2mentioning

confidence: 99%

See 1 more Smart Citation

Role of heat-shock factor 2 in cerebral cortex formation and as a regulatorof p35 expression

Chang¹,

Östling²,

Åkerfelt³

et al. 2006

Genes Dev.

109

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show abstract

“…KSR, kinase suppressor of ras; 1,25D 3 , 1,25-dihydroxyvitamin D 3 ; MEK1, mitogen-activated protein/extracellular signal-regulated kinase kinase 1; Erk, extracellular signal-regulated kinase. although the contribution of other transcription factors, such as Sp1 (43), cannot be excluded. Indeed, the GC boxes that can bind both Egr1 and Sp1 have been reported to act in concert (44).…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Egr1 by 1,25-Dihydroxyvitamin D3 Contributes to Increased Expression of p35 Activator of Cyclin-Dependent Kinase 5 and Consequent Onset of the Terminal Phase of HL60 Cell Differentiation

Chen¹,

Wang²,

Wang³

et al. 2004

Cancer Research

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“…The Sp4⌬ZnF mutant was generated by an inframe deletion of Sp4 amino acids 625-775. The reporter plasmid containing p35 promoter sequence Ϫ467 upstream of the luciferase gene has been described (45).…”

Section: Methodsmentioning

confidence: 99%

Transcription factor Sp4 regulates dendritic patterning during cerebellar maturation

Ramos

Gaudillière

Bonni

et al. 2007

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

Self Cite

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Integration of inputs by a neuron depends on dendritic arborization patterns. In mammals, the genetic programs that regulate dynamic remodeling of dendrites during development and in response to activity are incompletely understood. Here we report that knockdown of the transcription factor Sp4 led to an increased number of highly branched dendrites during maturation of cerebellar granule neurons in dissociated cultures and in cerebellar cortex. Time-course analysis revealed that depletion of Sp4 led to persistent generation of dendritic branches and a failure in resorption of transient dendrites. Depolarization induced a reduction in the number of dendrites, and knockdown of Sp4 blocked depolarization-induced remodeling. Furthermore, overexpression of Sp4 wild type, but not a mutant lacking the DNA-binding domain, was sufficient to promote dendritic pruning in nondepolarizing conditions. These findings indicate that the transcription factor Sp4 controls dendritic patterning during cerebellar development by limiting branch formation and promoting activitydependent pruning.branching ͉ dendrite ͉ depolarization ͉ pruning ͉ neuron T he nervous system is a complex and well coordinated network that depends on the formation of proper connections among diverse types of neurons. Dendritic arborization patterns determine the way a neuron integrates inputs. Defects in dendritic patterning correlate with severe neurodevelopmental disorders (1-3). Although proper dendritic arborizations are crucial for correct function of the nervous system, the genetic programs that govern dendritic morphology in mammals remain poorly described. Dendritic development is a highly dynamic process that involves many events, including neurite outgrowth, branching, stabilization, and pruning of dendrites (4-6). There is a delicate balance between addition and elimination of neuronal projections (7,8). During development, transient overproduction of branched dendrites appears in most neurons, after which some neurites are eliminated, whereas other neurites are stabilized to achieve the mature pattern (9-11). Recent studies have described intracellular signaling pathways that operate locally to regulate cytoskeletal elements important for branch formation or elimination (12)(13)(14).Extrinsic factors are coordinated with cell-intrinsic, gene expression programs to determine dendritic morphology. Genetic studies in Drosophila and Caenorhabditis elegans have identified transcription factors that regulate diverse aspects of dendritic morphology (15-18). Transcriptional control of the fine balance between formation and elimination of processes is illustrated by the finding that, in Drosophila, the homeodomain protein, Cut, promotes branching, whereas the BTB/POZ Zinc finger transcription, Abrupt, limits branch formation (18,19). In mammals, the transcriptional regulators CREB, NeuroD, and CREST have been identified to promote dendritic growth and branching (20-23). Transcriptional regulators that balance these activities to restrict dendritic branchin...

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GC Box-binding Transcription Factors Control the Neuronal Specific Transcription of the Cyclin-dependent Kinase 5 Regulator p35

Cited by 45 publications

References 78 publications

Role of heat-shock factor 2 in cerebral cortex formation and as a regulatorof p35 expression

Role of heat-shock factor 2 in cerebral cortex formation and as a regulatorof p35 expression

Up-Regulation of Egr1 by 1,25-Dihydroxyvitamin D3 Contributes to Increased Expression of p35 Activator of Cyclin-Dependent Kinase 5 and Consequent Onset of the Terminal Phase of HL60 Cell Differentiation

Transcription factor Sp4 regulates dendritic patterning during cerebellar maturation

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