The genes for human brain factor 1 and 2, members of the fork head gene family, are clustered on chromosome 14q

Wiese, Stefan; Murphy, Derek; Schlung, Astrid; Burfeind, Peter; Schmundt, Daphne; Schnülle, Volker; Mattei, M G; Thies, Ulrike

doi:10.1016/0167-4781(95)00059-p

Cited by 32 publications

(20 citation statements)

References 17 publications

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“…FOXG1B (NM_005249) showed a 100% identity to the genome sequence, whereas the other FOXG1B reference sequence, X74142, showed some discrepancies with a 163-nucleotide gap within the N-terminal domain and 45 nucleotide mismatches compared to the genome sequence. Additionally, the intron that FOXG1B was reported to contain (Wiese et al 1995) does not occur in the genomic sequence, as the mRNA sequence matches the genomic reference without any gaps. This was confirmed by PCR on human genomic DNA using primers that transversed the FOXG1B intron (Fig.…”

Section: Foxg1 Is Not Duplicated In Humansmentioning

confidence: 94%

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Comparative evolutionary analysis of the FoxG1 transcription factor from diverse vertebrates identifies conserved recognition sites for microRNA regulation

2007

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Comparative analysis of orthologues from diverse vertebrates can be used to identify molecular signatures that are important for gene function and which may predict novel regulatory mechanisms or explain morphological diversity. The forkhead box G1 (FoxG1) transcription factor is potentially a strong candidate gene for determining forebrain size in vertebrates due to its role in the development of the telencephalon, where it promotes progenitor proliferation and suppresses premature neurogenesis. To investigate the role of FoxG1 in forebrain evolution, we cloned and analyzed the cDNA sequences for nine new FoxG1 orthologues, including six mammals and three reptiles, and show that there is an extended proline and glutamine region in the N-terminal domain that is specific to mammals. In contrast to some previous studies of other potential determinants of brain size, we find no evidence that the coding sequence of FoxG1 has evolved under positive selection in vertebrates. Previously published work has indicated that FOXG1 was duplicated in humans, and two forms, FOXG1A and FOXG1B, are present in the Entrez Gene database. We report that FOXG1 has not been duplicated in humans and that FOXG1A is likely to be an artifact. Our comparative analysis of FOXG1B and its orthologues has revealed a very high level of conservation in the 3' untranslated region (UTR). Using available computational tools, we find evidence for conserved recognition sites for the miR-9 and miR-33 microRNAs in the FoxG1 3' UTR and hypothesize that these brain-expressed microRNAs may regulate FoxG1 post-transcriptionally during forebrain development.

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Section: Foxg1 Is Not Duplicated In Humansmentioning

confidence: 94%

“…As Wiese et al (1995) reported that FOXG1 had been duplicated in humans with FOXG1A and FOXG1B clustering on chromosome 14 (Fig. 3a), we investigated the hypothesis that the increased cortex size in humans may be a result of this duplication (Molnár et al 2006).…”

Section: Foxg1 Is Not Duplicated In Humansmentioning

confidence: 98%

Comparative evolutionary analysis of the FoxG1 transcription factor from diverse vertebrates identifies conserved recognition sites for microRNA regulation

2007

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“…some 4 kb (Wiese et al, 1995). It is reasonable to assume that this situation is due to a duplication, andas one would expect from a recent duplication eventthe predicted protein sequences are very similar (85% identity; Wiese et al, 1995). When the forkhead domains are compared it is evident that two amino acid substations are present (Wiese et al, 1995).…”

Section: Fig 5 a Human Poly(a)mentioning

confidence: 96%

“…Poly(A) / RNAs and control RNAs have been applied in the following order: A1, whole brain; A2, amygdala; A3, caudate nucleus; A4, cerebellum; A5, cerebral cortex; A6, frontal lobe; A7, hippocampus; A8, medulla oblongata; B1, occipital lobe; B2, putamen; B3, substantia niger; B4, temporal lobe; B5, thalamus; B6, subthalamic nucleus; B7, spinal cord; C1, heart; C2, aorta; C3, skeletal muscle; C4, colon; C5, bladder; C6, uterus; C7, prostate; C8, stomach; D1, testis; D2, ovary; D3, pancreas; D4, pituitary gland; D5, adrenal gland; D6, thyroid gland; D7, salivary gland; D8, mammary gland; E1, kidney; E2, liver; E3, small intestine; E4, spleen; E5, thymus; E6, peripheral leukocyte; E7, lymph node; E8, bone marrow; F1, appendix; F2, lung; F3, trachea; F4, placenta; G1, fetal brain; G2, fetal heart; G3, fetal kidney; G4, fetal liver; G5, fetal spleen; G6, fetal thymus; G7, fetal lung; H1, yeast total RNA (100 ng); H2, yeast tRNA (100 ng); H3, E. coli rRNA (100 ng). some 4 kb (Wiese et al, 1995). It is reasonable to assume that this situation is due to a duplication, andas one would expect from a recent duplication eventthe predicted protein sequences are very similar (85% identity; Wiese et al, 1995).…”

Section: Fig 5 a Human Poly(a)mentioning

confidence: 98%