ABSTRACT
Yeast TAF90p is a component of at least two transcription regulatory complexes, the general transcription factor TFIID and the Spt-Ada-Gcn5 histone acetyltransferase complex (SAGA). Broad transcription defects have been observed in mutants of other TAF(II)s shared by TFIID and SAGA but not in the only two TAF90 mutants isolated to date. Given that the numbers of mutants analyzed thus far are small, we isolated and characterized 11 temperature-sensitive mutants of TAF90 and analyzed their effects on transcription and integrity of the TFIID and SAGA complexes. We found that the mutants displayed a variety of allele-specific defects in their ability to support transcription and maintain the structure of the TFIID and SAGA complexes. Sequencing of the alleles revealed that all have mutations corresponding to the C terminus of the protein, with most clustering within the conserved WD40 repeats; thus, the C terminus of TAF90p is required for its incorporation into TFIID and function in SAGA. Significantly, inactivation of one allele, taf90-20, caused the dramatic reduction in the levels of total mRNA and most specific transcripts analyzed. Analysis of the structure and/or activity of both TAF90p-containing complexes revealed that this allele is the most disruptive of all. Our analysis defines the requirement for the WD40 repeats in preserving TFIID and SAGA function, demonstrates that the defects associated with distinct mutations in TAF90 vary considerably, and indicates that TAF90 can be classified as a gene required for the transcription of a large number of genes.
Subject(s)
Acetyltransferases/genetics , Mutation , Saccharomyces cerevisiae Proteins , TATA-Binding Protein Associated Factors , Transcription Factors, TFII/genetics , Transcription Factors/genetics , Transcription Factors/physiology , Transcription, Genetic , Acetyltransferases/metabolism , Alleles , Histone Acetyltransferases , Kinetics , Phenotype , Precipitin Tests , Protein Binding , Protein Structure, Tertiary , Temperature , Time Factors , Transcription Factor TFIID , Transcription Factors, TFII/metabolismABSTRACT
Critical flicker frequency (CFF) was determined for both eyes of long-term monocularly deprived (MD) cats over a wide luminance range. Although MD cats could discriminate flicker before and after lid opening, CFF of the deprived eye (30 Hz) was much lower than CFF of the non-deprived eye (40 Hz) and the CFF of the non-deprived eye was lower than a normal cat's monocular CFF (58 Hz). The CFF deficit of the deprived eye became less pronounced at low luminance levels. The observation (and magnitude) of a CFF deficit for the deprived eye is compatible with the reports of a Y-cell loss in LGNd. The CFF deficit of the non-deprived eye has no obvious explanation.
Subject(s)
Dominance, Cerebral/physiology , Flicker Fusion/physiology , Sensory Deprivation/physiology , Visual Pathways/physiology , Animals , Cats , Discrimination Learning/physiology , Female , Geniculate Bodies/physiology , Male , Pattern Recognition, Visual/physiology , Retinal Ganglion Cells/physiologySubject(s)
Form Perception , Adult , Female , Form Perception/physiology , Humans , Male , Reaction Time , Space Perception , Visual Cortex/physiologyABSTRACT
Critical flicker fusion was determined over a wide luminance range for six Siamese and four normal cats. The Siamese cats had the lowest CFF at all luminance levels when compared to normal and binocularly deprived (BD) cats. The Siamese cat's inferior temporal resolution is most likely due to their profound y-cell loss because (1) CFF is proportional to y-cell population across normal, BD, and Siamese cats; and (2) unlike BD cats, the visual cortex of Siamese cats is comparatively normal. The implication of this finding for the CFF of dark-reared cats and normal cats viewing a stimulus which does not stimulate y-cell is discussed.
