Transcription factors plate

Figure 2.21 Zinc-finger protein from the yeast transcription factors SWI as visualized using Wavefunction, Inc. Spartan 02 for Windows from PDB data deposited as 1NCS. See text for visualization details. Printed with permission of Wavefunction, Inc., Irvine, CA. (See color plate.)...

Figure 1. Schematics of the effect of mH2A on transcription, (a) The mobiUzation of conventional promoter nucleosome by the chromatin remodeling complex generated a nucleosome-free promoter, which allowed the binding of the transcription factors and transcription to proceed, (b) MacroH2A nucleosome cannot be mobilized by die chromatin remodeling complex and die transcriptions factors are unable to bind macroH2A nucleosome containing promoter, which results in inhibition of the initiation of transcription. (See Colour Plate 8.)...

Figure 2. Effect of H2A.Bbd on transcription. The presence of H2A.Bbd confers lower stability and more loose structure to the nucleosomes, which allows the transcription factors binding to this variant nucleosome and thereby recruitment of p300 and acetylation of the promoter proximal histones. The remodeling complex can not mobilize the variant nucleosome, but instead helps in the removal of H2A.Bbd-H2B dimer. All these events facilitate transcription. (See Colour Plate 9.)...

Figure I. Chromatin acetylation status, transcription and survival a balance between HAT and HDAC activities, (a) Transcriptional activationlrepression relies on the chromatin acetylation status of histones. TBP TATA-Binding Protein, TF Transcription Factor, TR Transcriptional Repressor, (b) A fine-tuning of HAT/HDAC activities orchestrates neuronal death and survival. On one hand, acetylation levels can be decreased (HypoAc) because of CBP loss of function, as observed during apoptosis and neurodegeneration. On the other hand, when the threshold of acetylation is exceeded (HyperAc), this ultimately leads to nemonal death. (See Colom Plate 16.)...

An important eukaryotic transcription factor is the nuclear factor, NF-kB (NF-xB). This factor binds to DNA through i-sheets. The i-sheets of the dimeric transcription factor wrap around the DNA like a mantle. Contacts are made, as in the case of a-helices, with die major groove of the DNA. The structure is shown in Plate 18. 

Finally, in Plate 21, the structure of the yeast TFIIA-TBP-DNA complex is shown. TFIIA interacts with TBP and the TFIID complex and stimulates transcription of the Pol II gene.29-32 TFIIA has two characteristic structural motife. One is a six-stranded (i-sand-wich, the other is a left-handed four-helix bundle. The P-sandwich domain of TFUA is alone responsible for all of the interactions with the DNA, whereas its helix-bundle domain projects away and is free to interact with signal-responsive transcription factors. These interactions are important for regulation of transcription. Little conformational change occurs in TBP when it binds to TFIIA. The main difference between the TFIIA-TPB complex and the TFIIB-TBP complex is that TFIIA binds upstream of the TATA box, away from the transcriptional start site, whereas TFIIB binds downstream of the TATA box. Moreover, TFIIB is positioned on the side opposite to TFIIA. 

Green, C.B., Durston, A.J., Morgan, R. 2001. The circadian gene Clock is restricted to the anterior neural plate early in development and is regulated by the neural inducer noggin and the transcription factor Otx2. Mech. Dev. 101, 105-110. 

The order in which various cell types arise is determined by the order in which transcription factors such as Hunchback, Kriippel, and others are expressed. Multipotential neural stem cells provide the new cells that are requiredNeural tissue from a region called the neural plate develops into a neural fold. 

---