Heat shock transcription factor (Hsf)‐4b recruits Brg1 during the G1 phase of the cell cycle and regulates the expression of heat shock proteins

Tu, Naxin; Hu, Yanzhong; Mivechi, Nahid F.

doi:10.1002/jcb.20865

Cited by 32 publications

(26 citation statements)

References 42 publications

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“…Transfected DNA mixes included 4 -8 g of expression plasmid DNA and, when required, empty plasmid DNA added to a total of 8 g. The DNA mixes were added to 5 ϫ 10 5 cells. The transfection efficiency varied between 60 and 70% in all experiments, as determined by immunofluorescence analysis Tu et al, 2006).…”

Section: Methodsmentioning

confidence: 99%

“…Cells were rinsed with PBS and resuspended in 400 l of PBS containing 20 l propidium iodide (1 mg/ml) and 2 l of RNase (50 mg/ml). After 30 min of incubation at 25°C, flow cytometric analyses were performed using CellQuest Pro with luminescence spectrophotometer (excitation at 480 nm and emission at 510 nm) (Tu et al, 2006).…”

Section: Methodsmentioning

confidence: 99%

“…Mouse embryo fibroblasts (MEFs) were prepared from embryonic day 13.5 (E13.5) after timed pregnancies. MEFs were transformed using plasmids containing SV40 large T antigen and were cultured in DMEM supplemented with 10% heat-inactivated fetal calf serum (FCS) (Tu et al, 2006). Cortical astrocyte cultures were established from postnatal day 2 mice.…”

Section: Methodsmentioning

confidence: 99%

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Demyelination, Astrogliosis, and Accumulation of Ubiquitinated Proteins, Hallmarks of CNS Disease inhsf1-Deficient Mice

Homma¹,

Jin²,

Wang³

et al. 2007

J. Neurosci.

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The heat shock transcription factors (Hsfs) are responsible for the heat shock response, an evolutionarily conserved process for clearance of damaged and aggregated proteins. In organisms such as Caenorhabditis elegans, which contain a single Hsf, reduction in the level of Hsf is associated with the appearance of age-related phenotypes and increased accumulation of protein aggregates. Mammalian cells express three hsfs (hsf1, hsf2, hsf4) and their role in CNS homeostasis remains unclear. In this study, we examined the effects of deletion of single or multiple hsf genes in the CNS using mutant mice. Our results show that hsf1 Ϫ/Ϫ mice display progressive myelin loss that accompanies severe astrogliosis and this is exacerbated in the absence of either the hsf2 or hsf4 gene. Magnetic resonance imaging and behavioral studies indicate reduction in the white matter tracts of the corpus callosum, and deficiencies in motor activity, respectively, in aged hsf1 Ϫ/Ϫ mice. Concomitantly, hsf1 Ϫ/Ϫ aged CNS exhibit increased activated microglia and apoptotic cells that are mainly positive for GFAP, an astrocyte-specific marker. Studies based on the expression of short-lived ubiquitinated green fluorescent protein (GFPu) in living hsf1Ϫ/Ϫ cells indicate that they exhibit reduced ability to degrade ubiquitinated proteins, accumulate short-lived GFPu, and accumulate aggregates of the Huntington's model of GFP containing trinucleotide repeats (Q103-GFP). Likewise, hsf1 Ϫ/Ϫ brain and astrocytes exhibit higher than wild-type levels of ubiquitinated proteins, increased levels of protein oxidation, and increased sensitivity to oxidative stress. These studies indicate a critical role for mammalian hsf genes, but specifically hsf1, in the quality control mechanisms and maintenance of CNS homeostasis during the organism's lifetime.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Demyelination, Astrogliosis, and Accumulation of Ubiquitinated Proteins, Hallmarks of CNS Disease inhsf1-Deficient Mice

Homma¹,

Jin²,

Wang³

et al. 2007

J. Neurosci.

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show abstract

“…c-Maf and Sox1 are joined by Hsf4 from E12.5 onward (Fujimoto et al, 2004;Min et al, 2004). As Hsf4 recruits Brg1, and, by inference the SWI/SNF complexes (Tu et al, 2006), it is possible that γ-crystallin promoters also use Brg1 for their chromatin remodeling.…”

Section: 23mentioning

confidence: 99%

Genetic and epigenetic mechanisms of gene regulation during lens development

Cvekl

Duncan

2007

Progress in Retinal and Eye Research

141

124

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Recent studies demonstrated a number of links between chromatin structure, gene expression, extracellular signaling and cellular differentiation during lens development. Lens progenitor cells originate from a pool of common progenitor cells, the pre-placodal region (PPR) which is formed due to a complex exchange of extracellular signals between the neural plate, naïve ectoderm and mesendoderm. A specific commitment to the lens program over alternate choices such as the formation of olfactory epithelium or the anterior pituitary is manifested by the formation of a thickened surface ectoderm, the lens placode. Mouse lens progenitor cells are characterized by the expression of a complement of lens lineage-specific transcription factors including Pax6, Six3 and Sox2, controlled by FGF and BMP signaling, followed later by c-Maf, Mab21like1, Prox1 and FoxE3. Proliferation of lens progenitors together with their morphogenetic movements results in the formation of the lens vesicle. This transient structure, comprised of lens precursor cells, is polarized with its anterior cells retaining their epithelial morphology and proliferative capacity, whereas the posterior lens precursor cells initiate terminal differentiation forming the primary lens fibers. Lens differentiation is marked by expression and accumulation of crystallins and other structural proteins. The transcriptional control of crystallin genes is characterized by the reiterative use of transcription factors required for the establishment of lens precursors in combination with more ubiquitously expressed factors (e.g. AP-1, AP-2α, CREB and USF) and recruitment of histone acetyltransferases (HATs) CBP and p300, and chromatin remodeling complexes SWI/SNF and ISWI. These studies have poised the study of lens development at the forefront of efforts to understand the connections between development, cell signaling, gene transcription and chromatin remodeling.

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“…ChIP assays were performed according to the previously published procedures (Takahashi et al, 2000;Tu et al, 2006). Zebrafish embryos were fixed at 12 and 22 hpf by the addition of one-tenth volume of formaldehyde in 0.l M NaCl, 1 mM EDTA, 0.5 mM EGTA, pH 8, 1 M HEPES, pH 8, and were placed on ice.…”

Section: In Vivo Cross-linking and Chromatin Immunoprecipitation (Chimentioning

confidence: 99%

Critical role of Brg1 member of the SWI/SNF chromatin remodeling complex during neurogenesis and neural crest induction in zebrafish

Eroglu

Wang

et al. 2006

Developmental Dynamics

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Brg1 is a member of the SWI/SNF chromatin-remodeling complex, and in some organisms Brg1 has been shown to interact with ␤-catenin and positively control the TCF/LEF transcription factor that is located downstream of the Wnt signal transduction pathway. During development, TCF/LEF activity is critical during neurogenesis and head induction. In zebrafish, Brg1-deficient embryos exhibit retinal cell differentiation and eye defects; however, the role of Brg1 in neurogenesis and neural crest cell induction remains elusive. We used zebrafish deficient in Brg1 (yng) or Brg1 specific-morpholino oligonucleotidemediated knockdown to analyze the embryonic requirements of Brg1. Our results indicate that reduction in Brg1 expression leads to the expansion of the forebrain-specific transcription factor, six3, and marked reduction in expression of the mid/hind-brain boundary and hind-brain genes, engrailed2 and krox20, respectively. At 12 hpf, the expression of neural crest specifiers are severely affected in Brg1-morpholinoinjected embryos. These results suggest that Brg1 is involved in neural crest induction, which is critical for the development of neurons, glia, pigment cells, and craniofacial structures. Brg1 is a maternal factor, and brg1-deficient embryos bearing the yng mutation derived from heterozygote intercrosses exhibit lesser effects on neural crest-specific gene expression, but show defects in neurogenesis and neural crest cell differentiation. This is exhibited by the aberrant brain patterning, a reduction in the sensory neurons, and craniofacial defects. These results further elucidate the critical role for Brg1 in neurogenesis, neural crest induction, and differentiation. Developmental Dynamics 235:2722-2735, 2006.

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Heat shock transcription factor (Hsf)‐4b recruits Brg1 during the G1 phase of the cell cycle and regulates the expression of heat shock proteins

Cited by 32 publications

References 42 publications

Demyelination, Astrogliosis, and Accumulation of Ubiquitinated Proteins, Hallmarks of CNS Disease inhsf1-Deficient Mice

Demyelination, Astrogliosis, and Accumulation of Ubiquitinated Proteins, Hallmarks of CNS Disease inhsf1-Deficient Mice

Genetic and epigenetic mechanisms of gene regulation during lens development

Critical role of Brg1 member of the SWI/SNF chromatin remodeling complex during neurogenesis and neural crest induction in zebrafish

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