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At least 451 records · Page 25Linked to original sources
PubMed2005

CPCR1, but not its interacting transcription factor AcFKH1, controls fungal arthrospore formation in Acremonium chrysogenum.

Fungal morphogenesis and secondary metabolism are frequently associated; however, the molecular determinants connecting both processes remain largely undefined. Here we demonstrate that CPCR1 (cephalosporin C regulator 1 from Acremonium chrysogenum), a member of the winged helix/regulator factor X (RFX) transcription factor family that regulates cephalosporin C biosynthesis, also controls morphological development in the beta-lactam producer A. chrysogenum. The use of a disruption strain, multicopy strains as well as several recombinant control strains revealed that CPCR1 is required for hyphal fragmentation, and thus the formation of arthrospores. In a DeltacpcR1 disruption strain that exhibits only hyphal growth, the wild-type cpcR1 gene was able to restore arthrospore formation; a phenomenon not observed for DeltacpcR1 derivatives or non-related genes. The intracellular expression of cpcR1, and control genes (pcbC, egfp) was determined by in vivo monitoring of fluorescent protein fusions. Further, the role of the forkhead transcription factor AcFKH1, which directly interacts with CPCR1, was studied by generating an Acfkh1 knockout strain. In contrast to CPCR1, AcFKH1 is not directly involved in the fragmentation of hyphae. Instead, the presence of AcFKH1 seems to be necessary for CPCR1 function in A. chrysogenum morphogenesis, as overexpression of a functional cpcR1 gene in a DeltaAcfkh1 background has no effect on arthrospore formation. Moreover, strains lacking Acfkh1 exhibit defects in cell separation, indicating an involvement of the forkhead transcription factor in mycelial growth of A. chrysogenum. Our data offer the potential to control fungal growth in biotechnical processes that require defined morphological stages for optimal production yields.

Acremonium↗
PubMed2004

Modulation of Th1 activation and inflammation by the NF-kappaB repressor Foxj1.

Forkhead transcription factors play key roles in the regulation of immune responses. Here, we identify a role for one member of this family, Foxj1, in the regulation of T cell activation and autoreactivity. Foxj1 deficiency resulted in multiorgan systemic inflammation, exaggerated Th1 cytokine production, and T cell proliferation in autologous mixed lymphocyte reactions. Foxj1 suppressed NF-kappaB transcription activity in vitro, and Foxj1-deficient T cells possessed increased NF-kappaB activity in vivo, correlating with the ability of Foxj1 to regulate IkappaB proteins, particularly IkappaBbeta. Thus, Foxj1 likely modulates inflammatory reactions and prevents autoimmunity by antagonizing proinflammatory transcriptional activities. These results suggest a potentially general role for forkhead genes in the enforcement of lymphocyte quiescence.

Animals↗
PubMed2006

Foxl2 up-regulates aromatase gene transcription in a female-specific manner by binding to the promoter as well as interacting with ad4 binding protein/steroidogenic factor 1.

Increasing evidence suggests the crucial role of estrogen in ovarian differentiation of nonmammalian vertebrates including fish. The present study has investigated the plausible role of Foxl2 in ovarian differentiation through transcriptional regulation of aromatase gene, using monosex fry of tilapia. Foxl2 expression is sexually dimorphic, like Cyp19a1, colocalizing with Cyp19a1 and Ad4BP/SF-1 in the stromal cells and interstitial cells in gonads of normal XX and sex-reversed XY fish, before the occurrence of morphological sex differentiation. Under in vitro conditions, Foxl2 binds to the sequence ACAAATA in the promoter region of the Cyp19a1 gene directly through its forkhead domain and activates the transcription of Cyp19a1 with its C terminus. Foxl2 can also interact through the forkhead domain with the ligand-binding domain of Ad4BP/SF-1 to form a heterodimer and enhance the Ad4BP/SF-1 mediated Cyp19a1 transcription. Disruption of endogenous Foxl2 in XX tilapia by overexpression of its dominant negative mutant (M3) induces varying degrees of testicular development with occasional sex reversal from ovary to testis. Such fish display reduced expression of Cyp19a1 as well as a drop in the serum levels of 17beta-estradiol and 11-ketotestosterone. Although the XY fish with wild-type tilapia Foxl2 (tFoxl2) overexpression never exhibited a complete sex reversal, there were significant structural changes, such as tissue degeneration, somatic cell proliferation, and induction of aromatase, with increased serum levels of 17beta-estradiol and 11-ketotestosterone. Altogether, these results suggest that Foxl2 plays a decisive role in the ovarian differentiation of the Nile tilapia by regulating aromatase expression and possibly the entire steroidogenic pathway.

Animals↗
PubMed2000

The FHA domain mediates phosphoprotein interactions.

The forkhead-associated (FHA) domain is a phosphopeptide-binding domain first identified in a group of forkhead transcription factors but is present in a wide variety of proteins from both prokaryotes and eukaryotes. In yeast and human, many proteins containing an FHA domain are found in the nucleus and involved in DNA repair, cell cycle arrest, or pre-mRNA processing. In plants, the FHA domain is part of a protein that is localized to the plasma membrane and participates in the regulation of receptor-like protein kinase signaling pathways. Recent studies show that a functional FHA domain consists of 120-140 amino acid residues, which is significantly larger than the sequence motif first described. Although FHA domains do not exhibit extensive sequence similarity, they share similar secondary and tertiary structures, featuring a sandwich of two anti-parallel (beta)-sheets. One intriguing finding is that FHA domains may bind phosphothreonine, phosphoserine and sometimes phosphotyrosine, distinguishing them from other well-studied phosphoprotein-binding domains. The diversity of proteins containing FHA domains and potential differences in binding specificities suggest the FHA domain is involved in coordinating diverse cellular processes.

Arabidopsis↗
PubMed2006

Foxp3 represses retroviral transcription by targeting both NF-kappaB and CREB pathways.

Forkhead box (Fox)/winged-helix transcription factors regulate multiple aspects of immune responsiveness and Foxp3 is recognized as an essential functional marker of regulatory T cells. Herein we describe downstream signaling pathways targeted by Foxp3 that may negatively impact retroviral pathogenesis. Overexpression of Foxp3 in HEK 293T and purified CD4+ T cells resulted in a dose-dependent and time-dependent decrease in basal levels of nuclear factor-kappaB (NF-kappaB) activation. Deletion of the carboxyl-terminal forkhead (FKH) domain, critical for nuclear localization and DNA-binding activity, abrogated the ability of Foxp3 to suppress NF-kappaB activity in HEK 293T cells, but not in Jurkat or primary human CD4+ T cells. We further demonstrate that Foxp3 suppressed the transcription of two human retroviral promoters (HIV-1 and human T cell lymphotropic virus type I [HTLV-I]) utilizing NF-kappaB-dependent and NF-kappaB-independent mechanisms. Examination of the latter identified the cAMP-responsive element binding protein (CREB) pathway as a target of Foxp3. Finally, comparison of the percent Foxp3+CD4+CD25+ T cells to the HTLV-I proviral load in HTLV-I-infected asymptomatic carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis suggested that high Foxp3 expression is associated with low proviral load and absence of disease. These results suggest an expanded role for Foxp3 in regulating NF-kappaB- and CREB-dependent cellular and viral gene expression.

CD4-Positive T-Lymphocytes↗
PubMed2005

Restraint of B cell activation by Foxj1-mediated antagonism of NF-kappa B and IL-6.

The forkhead transcription factor Foxj1 inhibits spontaneous autoimmunity, in part by antagonizing NF-kappaB activation in T cells. We demonstrate here that Foxj1 also inhibits humoral immune responses intrinsically in B cells; Foxj1 deficiency in B cells results in spontaneous and accentuated germinal center formation, associated with the development of pathogenic autoantibodies and accentuated responses to immunizations-all reflecting excessive activity of NF-kappaB and its target gene IL-6, and correlating with a requirement for Foxj1 to regulate the inhibitory NF-kappaB component IkappaBbeta. Thus, Foxj1 restrains B cell activation and the maturation of humoral responses, demonstrating a critical role for at least this forkhead transcription factor in the regulation of B lymphocyte homeostasis.

Animals↗
PubMed2006

FOXO transcription factors cooperate with delta EF1 to activate growth suppressive genes in B lymphocytes.

Forkhead transcription factors regulate many aspects of lymphocyte development and function. The FOXO subgroup of Forkhead factors opposes proliferation and survival, and FOXO inactivation is an important outcome of Ag receptor signaling. FOXO activity at target promoters is modulated by other transcription factors in a manner dependent on cell type and external stimulus. We have investigated the mechanisms by which FOXO proteins activate the promoters of two target genes in murine B lymphocytes, Ccng2 (encoding cyclin G2) and Rbl2 (p130), each of which has been implicated in cell cycle arrest. FOXO proteins bound directly to both promoters in vitro and in vivo, augmented transcriptional activity in reporter assays, and increased expression of the endogenous genes. Each of the promoter sequences has consensus binding sites for the deltaEF1 transcription factor, previously shown to either repress or activate different promoters. deltaEF1 bound to the Ccng2 and Rbl2 promoters in vitro and in vivo and increased reporter activity as well as endogenous mRNA levels for these genes. Strikingly, deltaEF1 synergized with FOXO proteins to strongly activate transcription from both promoters. Coexpression of deltaEF1 enhanced FOXO-induced cell cycle arrest in B lymphoma cells. These findings establish a novel mechanism of FOXO function at target promoters: cooperation with deltaEF1.

Animals↗
PubMed2002

Foxe3 haploinsufficiency in mice: a model for Peters' anomaly.

PURPOSE: To evaluate the importance in anterior segment dysgenesis of genetic variation in Foxe3, a gene encoding a forkhead transcription factor specifically expressed in the lens. METHODS: The phenotype of mice heterozygous for a mutation in the DNA-binding domain of Foxe3 was examined from histologic sections, and DNA binding by the encoded protein was investigated by gel-shift assay. FOXE3 from human patients with Peters' anomaly was PCR amplified and sequenced. RESULTS: The dysgenetic lens (dyl) allele of Foxe3 was found to encode a protein unable to bind DNA. Approximately 40% of mice heterozygous for Foxe3(dyl) have corneal and lenticular defects. The phenotype is variable but typically consists of the equivalent of Peters' anomaly in humans, with central corneal opacity, keratolenticular adhesion, and, in some cases, anterior polar cataract. In a small cohort (n = 13) of patients with Peters' anomaly, shown to be normal in the PAX6 locus, one individual was found to be heterozygous for a nonconservative missense mutation in FOXE3. The mutation, which does not occur in 116 chromosomes from a control population, substitutes leucine for arginine 90 at a highly conserved position in the forkhead domain. CONCLUSIONS: Haploinsufficiency of Foxe3 in a mouse model causes anterior segment dysgenesis similar to Peters' anomaly. Although causality could not be shown in the human case, the presence of a rare, nonconservative substitution in FOXE3 of a patient with Peters' anomaly is interesting, in light of the phenotypic similarities with the mutant mice.

Amino Acid Sequence↗
PubMed2004

Identification and characterization of human FOXN5 and rat Foxn5 genes in silico.

Forkhead-box (FOX) genes are implicated in embryogenesis through transcriptional regulation depending on SHH-GLI pathway, TGF-beta pathway etc., and also in carcinogenesis through gene amplification, retroviral integration and chromosomal translocation. FOXN1, FOXN2 (HTLF), FOXN3 (CHES1) and FOXN4 constitute the FOXN family. Here, we identified and characterized the FOXN5 gene, a novel member of FOXN gene family, by using bioinformatics. IMAGE5167039 (BC028191.1) was the representative cDNA derived from human FOXN5 gene. Rat Foxn5 gene, consisting of six exons, was identified within rat genome sequence CH230-26K11 (AC107575.5). Complete coding sequence of rat Foxn5 cDNA was determined by assembling nucleotide sequences of rat Foxn5 exons. Human FOXN5 (292 aa) and rat Foxn5 (296 aa) showed 77.4% total-amino-acid identity. Codon 173-254 of FOXN5 was the Forkhead domain. FOXN5 gene, consisting of six exons, was linked to BCL9L gene at human chromosome 11q23.3. FOXN5 is a candidate tumor suppressor gene (TSG), just like ARHGAP20 (KIAA1391), BTG4, SNF1LK2 (SIK2), DIXDC1 (KIAA1735) genes at 11q23.1, TTC12 (TPARM) gene at 11q23.2, IGSF4, DSCAML1, LL5A (PHLDB1), BCL9L, RNF26, and MFRP genes at 11q23.3. This is the first report on the human FOXN5 and rat Foxn5 genes.

Amino Acid Sequence↗
PubMed2004

Identification and characterization of human FOXN6, mouse Foxn6, and rat Foxn6 genes in silico.

Forkhead-box (FOX) transcription factors are implicated in carcinogenesis through gene amplification, retroviral integration, or chromosomal translocation. FOXN1, FOXN2 (HTLF), FOXN3 (CHES1), FOXN4 and FOXN5 (FOXR1) constitute the FOXN family. Here, we identified and characterized human FOXN6 (FOXR2) and rodent Foxn6 (Foxr2) orthologs by using bioinformatics. Human FOXN6 gene was identified within human genome sequence RP11-167P23 (AL159987.19), mouse Foxn6 gene within mouse genome sequence RP23-180D16 (AL672293.14), and rat Foxn6 gene within rat genome sequence CH230-264B14 (AC106980.5). FOXN6, RRAGB (RAGB), and KLF8 genes were clustered at human chromosome Xp11.21. Foxn6, Rragb, and Klf8 genes were also clustered at mouse chromosome XF3 as well as at rat chromosome Xq14. Human FOXN6 mRNA was expressed in breast cancer cell line and primary breast cancer. Mouse Foxn6 mRNA was expressed in E9.5 embryo. Human FOXN6 (286 aa) showed 57.7% total-amino-acid identity with human FOXN5, 53.8% total-amino-acid identity with mouse Foxn6 (277 aa), and 52.4% total-amino-acid identity with rat Foxn6 (277 aa). Codon 167-248 of human FOXN6 was the Forkhead domain. FN56 domain (codon 1-69 of FOXN6) was identified as a novel domain conserved among FOXN6 and FOXN5 orthologs. Mammalian FOXN6 orthologs were found consisting of FN56 and FOX domains. Phylogenetic analyses revealed that FOXN family proteins are classified into three subfamilies: i) FOXN6 and FOXN5 orthologs; ii) FOXN1 and FOXN4 orthologs; iii) FOXN2 and FOXN3 orthologs. This is the first report on human FOXN6, mouse Foxn6, and rat Foxn6 genes.

Amino Acid Sequence↗
PubMed2004

Identification and characterization of human FOXK1 gene in silico.

Forkhead-box (FOX) family transcription factors are implicated in carcinogenesis and embryogenesis. Here, we identified and characterized the human FOXK1 gene by using bioinformatics. Complete coding sequence of human FOXK1 cDNA was determined by assembling CB959941 EST, AW206906 EST, and 5'-truncated FLJ16099 (AK122663.1) cDNA. FOXK1 gene, consisting of nine exons, was mapped to human chromosome 7p22.1. Mouse Foxk1 (NM_199068.1) was an aberrant cDNA with frame shifts due to multiple insertions and deletions, while mouse IMAGE6853263 (BC060238.1) was a Foxk1 cDNA with a frame shift due to two base deletions. Complete coding sequence of mouse Foxk1 cDNA was determined by inserting CA nucleotides between nucleotide position 1628 and 1629 of BC060238.1. Foxk1 gene, consisting of nine exons, was mapped to mouse chromosome 5G2. Because interleukin enhancer-binding factor 1 (ILF1) gene at human chromosome 17q25.3 was the paralog of FOXK1 gene, ILF1 gene was designated the FOXK2 gene. Xenopus BC046369.1 cDNA was Foxk2 ortholog rather than Foxk1 ortholog. Human FOXK1 (733 aa) showed 88.7% total amino-acid identity with mouse Foxk1 (719 aa), 48.7% total amino-acid identity with human FOXK2, and 47.5% total amino-acid identity with Xenopus Foxk2. Forkhead associated (FHA) domain and FOX domain were conserved among human FOXK1, FOXK2, mouse FoxK1, and Xenopus Foxk2. At least 42 FOX family genes, including FOXK1, FOXN5 (FOXR1) and FOXN6 (FOXR2), have been identified within the human genome.

Amino Acid Sequence↗
PubMed2004

Identification and characterization of a novel human FOXK1 gene in silico.

We describe here the identification and characterization of a human forkhead box gene, FOXK1, that encodes predicted proteins most homologous to the mouse myocyte nuclear factor (MNF)/forkhead box K1 (FoxK1). Human FOXK1 is located at the chromosomal position 7p22. Two transcript variants, FOXK1a and FOXK1b, containing the divergent 5'-ends are identified. Sequence comparison indicated that the human FOXK1 proteins share 66-74% amino acid identity (99% identity in the forkhead domain) with their mouse ortholog. The in silico expression analysis showed FOXK1 expression in immature tissues of brain, eye, heart, lung and thymus. In adults, FOXK1 was predominantly expressed in many malignant tissues, in particular in the tumors of brain, colon and lymph node. This gene is therefore implicated in the process of both normal and neoplastic development.

Amino Acid Sequence↗
PubMed1996

The diagnostic potential of the chromosome translocation t(2;13) in rhabdomyosarcoma: a Pcr study of fresh-frozen and paraffin-embedded tumour samples.

The chromosomal translocation t(2;13)(q35;q14) has been reported in alveolar paediatric rhabdomyosarcoma. The rearrangement leads to the juxtaposition of the PAX-3 and FORKHEAD genes and the production of a fusion protein with putative transcriptional regulatory activity. The diagnostic potential of this translocation has been examined using a reverse transcription polymerase chain reaction (RT-PCR) assay to detect translocations in both fresh-frozen and archival formalin-fixed, paraffin-embedded rhabdomyosarcoma. A total of 25 tumours and one cell line were examined. PAX-3-FORKHEAD chimeric mRNAs were amplified by PCR in 8 of 15 cases of alveolar rhabdomyosarcoma. Translocations were detectable in both fresh-frozen tissues (4 of 7) and paraffin-embedded tumours (3 of 7) and in the alveolar rhabdomyosarcoma cell line. Our study confirms that the t(2;13) translocation is not present in embryonal rhabdomyosarcomas, but can be detected in nearly half of alveolar rhabdomyosarcomas, whether fresh-frozen or paraffin-embedded. The PCR-based t(2;13) translocation assay can aid in the diagnosis of rhabdomyosarcoma, but cannot replace a careful histopathological evaluation. It may contribute in further characterizing an otherwise undifferentiated small cell tumour, where it may be indicative of clinical behaviour.

Blotting, Southern↗
PubMed2005

alpha5beta1 integrin stimulates Bcl-2 expression and cell survival through Akt, focal adhesion kinase, and Ca2+/calmodulin-dependent protein kinase IV.

CHO cells expressing alpha5beta1 integrin are more resistant to apoptosis and express more Bcl-2 than the same cells engineered to express alphavbeta1 or cytoplasmically truncated alpha5Deltacbeta1 integrin as their main fibronectin receptor. The Bcl-2 up-regulation by alpha5beta1 is mediated, at least in part, by the focal adhesion kinase (FAK) and phosphatidylinositol-3 kinase (PI3K)/Akt pathways. Here, we show that integrin-mediated activation of Ca2+/calmodulin-dependent protein kinase (CaMK) IV, and the NF-kappaB and CREB transcription factors also enhance the integrin-dependent regulation of Bcl-2 expression in the alpha5beta1cells. A forkhead transcription factor, which is inactivated by Akt, blocked Bcl-2 expression. The FAK pathway was found to be defective in both the alphavbeta1 and alpha5Deltacbeta1 cells. These cell lines differed from one another in two Bcl-2-regulating pathways: adhesion through alphavbeta1 failed to activate Akt, allowing forkhead to suppress Bcl-2 transcription, whereas alpha5Deltacbeta1 did not activate NF-kappaB and CREB, presumably because CaMK IV was not activated. Our results indicate that three pathways, the FAK, PI3K/Akt, and CaMK IV mediate the survival-supporting activity of alpha5beta1 integrin.

Animals↗
PubMed2005

Homeobox B3, FoxA1 and FoxA2 interactions in epithelial lung cell differentiation of the multipotent M3E3/C3 cell line.

HOM/C homeobox (Hox) and forkhead box (Fox) factors are reported to be expressed in the foregut endoderm and are subsequently detected in a spatio-temporal pattern during lung development. Some of these factors were reported to influence the expression of lung marker proteins or to modulate lung development. To clarify the molecular mechanisms for generating functional lung cells from progenitor cell populations, we introduced the forkhead box factors, FoxA1 and FoxA2, and the homeobox factor, HoxB3, into the differentiation process in a multipotent hamster lung epithelial M3E3/C3 cell line. Ectopic expression of FoxA2 promoted differentiation to Clara-like cells with up-regulation of the expression of the lung marker proteins, Clara cell-specific 10-kDa protein and surfactant protein-B. In contrast, FoxA1 repressed the differentiation. HoxB3 transfection induced FoxA2 expression transiently at the pre-differentiation stage. The endogenous HoxB3 expression level decreased at later stages of Clara-like cell differentiation, and the attenuation was enhanced by FoxA2 transfection. HoxB3 is a putative upstream regulator that enhances FoxA2 expression at the pre-differentiation stage. In addition, we found that the expression of HoxA4, HoxA5, and HoxC9 increased differentially during Clara-like cell differentiation. These results suggest that HoxB3 may be a putative positive regulator of FoxA2 expression at the pre-differentiation stage, and those interactions of Fox factors and Hox factors could participate in Clara cell differentiation.

Animals↗
PubMed2006

Are regulatory T-cells linked with aging?

There is increasing evidence for an active and 'dominant' tolerance mediated by regulatory T-cells. Out of these CD4+ 'naturally occurring' regulatory T-cells (TREGs) are currently the main research focus in this field. TREGs exert their suppressive function in vitro in a contact-dependent manner and preferentially express high levels of CD25 and the forkhead and winged-helix family transcription factor forkhead box P3 (FOXP3). Age-related increment of the prevalences of CD4+ CD25(hi) TREGs were described controversially, and whether such changes explain immune dysfunction in the elderly is still unclear. During aging thymic TREG output may decrease with significant loss of thymic capacity to generate new T-cells, and TREG homeostasis has been shown to be sustained by alternative pathways like peripheral generation of TREGs. An imbalance of TREG homeostasis would then predispose to immune dysfunction in aged individuals explaining their higher risk of immune-mediated diseases, cancer or infections.

Aging↗
PubMed2005

The amphioxus FoxQ1 gene is expressed in the developing endostyle.

The FoxQ1 genes form a distinct group within the Fox (also known as forkhead) gene family. We have isolated a gene from the amphioxus Branchiostoma floridae that encodes a forkhead domain with high identity to FoxQ1 genes in other chordates. Molecular phylogenetic analysis places AmphiFoxQ1 in a robust grouping with vertebrate FoxQ1 genes and with Ciona intestinalis Ci-FoxQ1. This group is separate from that containing AmphiFoxQ2, which instead groups with other invertebrate Fox genes. The expression of AmphiFoxQ1 was analysed by whole mount in situ hybridisation. The results show that AmphiFoxQ1 expression is confined to the developing endoderm, and specifically marks the endostyle and associated peripharyngeal bands of amphioxus larvae. Ci-FoxQ1 is also expressed in the endostyle, highlighting this as a conserved site of FoxQ1 gene expression in basal chordates.

Animals↗
PubMed2004

FoxA1 binding to the MMTV LTR modulates chromatin structure and transcription.

Novel binding sites for the forkhead transcription factor family member Forkhead box A (FoxA), previously referred to as Hepatocyte Nuclear Factor 3 (HNF3), were found within the mouse mammary tumor virus long terminal repeat (MMTV LTR). The effect of FoxA1 on MMTV LTR chromatin structure, and expression was evaluated in Xenopus laevis oocytes. Mutagenesis of either of the two main FoxA binding sites showed that the distal site, -232/-221, conferred FoxA1-dependent partial inhibition of glucocorticoid receptor (GR) driven MMTV transcription. The proximal FoxA binding segment consisted of two individual FoxA sites at -57/-46 and -45/-34, respectively, that mediated an increased basal MMTV transcription. FoxA1 binding altered the chromatin structure of both the inactive- and the hormone-activated MMTV LTR. Hydroxyl radical foot printing revealed FoxA1-mediated changes in the nucleosome arrangement. Micrococcal nuclease digestion showed the hormone-dependent sub-nucleosome complex, containing approximately 120 bp of DNA, to be expanded by FoxA1 binding to the proximal segment into a larger complex containing approximately 200 bp. The potential function of the FoxA1-mediated expression of the MMTV provirus for maintenance of expression in different tissues is discussed.

Animals↗