* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Eukaryotic Gene Regulation
Molecular cloning wikipedia , lookup
Deoxyribozyme wikipedia , lookup
Protein moonlighting wikipedia , lookup
Genomic imprinting wikipedia , lookup
Cre-Lox recombination wikipedia , lookup
Secreted frizzled-related protein 1 wikipedia , lookup
Histone acetylation and deacetylation wikipedia , lookup
List of types of proteins wikipedia , lookup
Community fingerprinting wikipedia , lookup
Genome evolution wikipedia , lookup
Expression vector wikipedia , lookup
Gene expression profiling wikipedia , lookup
Non-coding DNA wikipedia , lookup
Molecular evolution wikipedia , lookup
Promoter (genetics) wikipedia , lookup
Point mutation wikipedia , lookup
Gene regulatory network wikipedia , lookup
Vectors in gene therapy wikipedia , lookup
Gene expression wikipedia , lookup
Transcriptional regulation wikipedia , lookup
Eukaryotic Gene Regulation Chromatin Structure DNA & protein 1) Nucleosomes DNA & histones (proteins) DNA wrapped around 8-piece histone bead Chromatin Structure 2) 30-nm chromatin fiber 3) Looped domains Fiber loops around scaffold of nonhistone proteins 4) Metaphase chromosome Further folding & coiling to compact Chromatin Structure In interphase, compacted chromatin: heterochromatin (not transcribed – proteins can’t reach the DNA) Non-compacted: euchromatin (is transcribed) Genomic Organization Gene Rearrangement Loss or shuffling of genome Change loci of genes in somatic cells Transposons If it “jumps” into middle of a coding sequence, it stops normal function Itself can be activated if near active promotor Genomic Organization 10% of human genome, but many are retrotransposons Move by means of RNA intermediate & reverse transcriptase Process like retroviruses Control of Gene Expression Cellular Differentiation Become specialized for a function Only fraction of genes turned on (3-5%) Regulated at transcription by DNAbinding proteins that receive internal & external signals Control of Gene Expression Chemical modification of chromatin also regulates transcription 1)DNA methylation Attachment of -CH3 groups to DNA bases (cytosine) after DNA synthesis Inactive DNA is highly methylated (removing can possibly activate genes) Control of Gene Expression Once methylated, tend to stay that way through cell divisions The pattern is passed on – form of genomic imprinting (it permanently turns off maternal or paternal allele) Control of Gene Expression 2)Histone Acetylation Attachment of acetyl groups (-COCH3) to amino acids of histones Changes their shape – grip DNA less Easier to transcribe that section of DNA Control of Gene Expression 3) Control elements Noncoding DNA regulating transcription Proximal control elements – promotor Control of Gene Expression Distal control elements (farther away) – enhancers Causes DNA to bend so transcription factors (activators) bound to enhancers can contact proteins of TIC of promoter Repressors bind to control elements known as silencers (much less common) Control of Gene Expression Coordination Need to turn genes of related function on or off at same time No operons like prokaryotes Each gene has own promotor, so how to coordinate? Copies of transcription factors associate with specific control elements of related genes – they activate by same signal (through signal-transduction pathways), bind, & transcribe simultaneously Control of Gene Expression 4) mRNA Degredation 5) Translation initiation Blocked by proteins that bind to 5’ end of mRNA so ribosome cannot attach Control of Gene Expression 6) Protein processing & degradation After translation During modification or transport of protein FYI…To destruct protein, it is marked with a protein ‘tag’ (ubiquitin); proteasomes recognize this & degrade the protein Cancer Cancer-causing genes: oncogenes From retroviruses Normal gene – proto-oncogene Normal becomes cancer in three ways: Movement of DNA within genome Amplification of proto-oncogene Point mutation of proto-oncogene Cancer Tumor-suppressor genes Prevent uncontrolled growth If damaged, cancer could result Typical jobs: repair damaged DNA to prevent improper accumulation Control cell anchorage (absent in cancer) Cancer Genes often involved: 1) ras – mutated in 50% of cancers Uses signal-transduction pathway Ras is a G protein – end result – synthesis of protein to stimulate cell cycle Oncogene can work without growth factor due to point mutation (issues signals by itself) Cancer 2) p53 gene – mutated in 30% of cancers S-T-pathway that makes protein that inhibits cell cycle Uses many ways to prevent cell from passing on mutations from DNA damage Damage to gene no inhibition cancer