The genetic map of bacteriophage The genetic map of bacteriophage
Control of transcription in bacteriophage life cycle by the anti-terminators N and Q proteins, the activator C II protein and the repressor/activator C I protein
Characteristics of diploid with gal80, gal4, and GAL81c mutations Mutations affecting galactose pathway in yeast: Genotype Synthesis of GAL1,GAL7,and GAL10 RNAs Gal phenotype gal80, GAL1/GAL80 GAL1 Inducible+ gal4 GAL1/GAL4 GAL1 (gal4/gal4 uninducible) Inducible+ GAL81 c GAL1/GAL81 GAL1 Constitutive+
The steps and enzymes involved in the utilization of the sugar galactose in the yeast Saccharomyces
The transcriptional orientation of the 3 genes coding for enzymes important in galactose utilization in Saccharomyces There synthesis is regulated by the transcription activator Gal4 protein.
GAL4 bound to DNA
A protein with a C 6 -zinc finger (involves 6 cysteines) Many transcription regulator proteins have one (or more) zinc-finger domains
A retrovirus genome showing the location of the transcription activation sites (enhancers) The genome structure of mouse mammary tumor virus is shown here
Analysis of genetic regulation using reporter gene constructs
A transcription activator protein binds to the enhancer site and also interacts with components of the RNA polymerase to achieve increased transcription Enhancers and enhancer- binding proteins activate transcription reminiscent of the CAP site and CRP activator protein in the lac operon of E. coli.
Structures like this involving DNA with bound activator proteins and RNA polymerase complex are names “enhanceosomes”. TBP stands for TATA- binding protein, a component of RNA polymerase II associated factor, TFIID A model for the structure of activator proteins bound to 2 enhancers and RNA polymerase II bound to the promoter and the interactions between them
Uncovering of transcription protein binding sites by chromatin remodeling complexes makes binding by transcription-proteins possible
Use of alternative promoters at different stages in life
Different promoters may be enhanced depending upon which activator protein is present in a cell
Alternative splicing of the primary transcript
Structure of an immunoglobulin G (IgG) molecule
The distribution of variable, joining and constant sequences which are spliced to create many different light chain proteins
Mating type switching during the life cycle of some strains of Saccharomyces
Both mating type genes are located on chromosome III of Saccharomyces. The mating type of the cell is determined by the sequence present at the MAT site
Regulation of a-specific, -specific and haploid-specific genes in Saccharomyces Three proteins (a1, 1 and 2) are involved in regulating the expression of these 3 classes of genes.
Cutting by methylcytosine sensitive/insensitive restriction nucleases can be used to estimate the extent of cytosine methylation in a DNA sequence
Imprinted genes in mammals Table 2. Human imprinted genes and their mouse orthologues a (tab002gml) Human gene Human chromosome Mouse gene Mouse chromosome NOEY2, ARH11p31 p731p36.33 ZAC, PLAGL16q24Zac1, Lot110 HYMA16q24.1-q24.3 IGF2R, M6PR b 6q25.3Igf2r17 GRB10, MEG17p11.2-p12Grb10, Meg111 MEST, PEG17q32Peg1, Mest6 COPG2 b 7q32Copg26 WT1 b 11p13 H1911p15.5H197 IGF211p15.5Igf27 INS11p15.5Ins2, insulin II7 ASCL2, HASH211p15.5 LTRPC5, MTR111p15.5 KCNQ1, KVLQT111p15.5Kcnq1, Kvlqt17 CDKN1C, p57 KIP2 11p15.5Cdnk1c, p57, Kip27 TSSC5, SLC22A1L11p15.5Orct12, Impt1, Itm, Tssc5, Bwscr1a7 IPL, TSSC311p15.5Tssc37 ZNF21511p15.5 2G3-811p15.5 SDHD11q22.3-q23 HTR2A13q4Htr2a14 MEG3, GTL214q32Meg3, Gtl212 DLK1, PEG914q32Dlk1, pref1, Ly107, FA1, SCP1, Zog, Peg912 MKRN, ZNF12715q11-q13 NDN15q11-q13Ndn, nectin7 MAGEL2, NDNL115q11-q13 SNURF-SNRPN15q11-q13Snrpn7 PAR-SN15q11-q13 HBII-1315q11-q13 HBII-85, PWCR115q11-q13 HBII-5215q11-q13 PAR515q11-q13 PAR115q11-q13 IPW15q11-q13Ipw7 UBE3A15q11-q13Ube3a7 ATP10C15q11-q13 GABRB315q11-q13Gabrb37 GABRA515q11-q13Gabra57 GABRG315q11-q13Gabrg37 PEG319q13.4Peg3, Pw17 GNAS120q13.11Gnas2 XISTXXist, TsixX a Adapted from b Imprinting status disputed. Antisense transcripts have not been included.
Some human diseases are due to loss of sites involved in genomic imprinting
Alternative splicing of mRNA
Nonsense-mediated decay of mRNA
Alt.splicing combined with NMD can be used for genetic control
RNAi (RNA interference): dsRNA directs degradation of mRNA with the same/complementary sequence
Translational control