Week 7 Finish 9, 10 and 11
How do we measure gene expression? In order to check if it is expressed we need.... what are 6 methods for measuring transcription?
-USUALLY use methods that analyze mRNA levels "how much of a transcript exists at a certain time or tissue" In order to check if it is expressed we need mRNA that is already been processed (partially or fully) 6 methods: 1) northern blotting 2) Run On Assays 3) Reporter gene assay 4) RT-PCR 5) micro arrays 6) RNA seq
What are the multiple functions of the POLY A TAIL for the pre-mature-mRNA?
1) - enhances transport of mRNA to cytoplasm by being recognized by specific transport proteins. 2) - enhances translation of mRNA. 3) - protects mRNA from degradation. - 4) helps identify RNAs for degradation. >> RNA is somewhat unstable RNAs with short polyA tails (or no tail) are more susceptible to RNAses so basically all of the 5' cap except it doesnt help for splicing, instead helps ID RNA for degradations
What are the two main types of readers and what do they contain how can this effect chromatin on a large scale
1) Bromodomain containing proteins: >> Consist of 1) HAT writers, TAFS, NUCLEOSOME remodeling complexes, other transcriptional regulators 2) Chromodomain containing protein: >> 1) consist of Histone methylate writers; 2) heterochromatin and 3) nucleosome remodeling complexes 4) transcriptional regulators can affect chromatin on a larger scale by spreading chromatin changes along the chromosome (large condensing or loosening)
what proteins are needed for the 3' poly A tail and explain what they all do and if needed, where they bind to on the mRNA
1) CPSF- Cleavage and poly A specific factor BINDS to the AAUAAA sequence 2) CF1 & 2 bind inbetween the AAUAAA and GU region 3) CStF Cleavage and stimulation factor directly binds to the GU THIS IS WHAT ALLOWS THE SITE TO BE CLEAVED after the AAUAAA region 4) PAP- poly adenylation polymerase= makes about 10 adenines but then 4)PAB- poly A binding protein comes in and helps it make even more adenines
what does capping do for the mRNA (list the functions, there are multiple)
1) Enhances transport of the mRNA to the cytoplasm by transport proteins (and proteins specifically binding to the cap) 2) Enhances translation of mRNA (the 5'cap recruits translation machinery) 3) Enhances proper splicing of pre-mRNA (interacting with the spliceosome) 4) Protects mRNA from degradation 1) DIRECTLY via blocking guanine and proteins 2) INDIrect- the enhanced ribosomal bindings make it so the ribonucleases (exo and endo) dont find and attack it
What are the applications and uses of cDNA?
1) Express an "intron bearing gene in bacteria" meaning it had introns before, but now it doesnt because bacteria cannot remove them 2) compare cDNA to genomic DNA to map out introns 3) Measure the levels of gene expression via RT_QPCR 4) produce an animal protein, and express it in bacteria because it will no longer have the introns 5) Make a library of all the expressed genes to show all the mRNA in the cell. Can give gene specific info
For the modification enzymes: What are the histone modification enzymes for acetylation (explain their action)
1) HATS: Histone acetyl transferases - directly acetylates the histone mark at the lysine residues 2) Histone deacetylase (HDAC) : catalyze the removal of acetyl groups for proper regulation
For the modification enzymes: What are the histone modification enzymes for methylation (explain their action)
1) Histone methyl transferase - Methylate histone at lysine and arginine 2) Histone demethylase (LSD-1) - remove em (lysine specific)
explain the 7 steps of using cDNA to clone in a bacteria
1) Isolate all the mRNA -seperate the mRNA from other types of non mRNA with POLY T BEADS 2) the string of T's= primer for the CDNA= use RTASE to made a CDNA-RNA hybrid 3) Use a G tail to the DNA made with terminal transferase GTP and place it on te 3' end of the same strand with all the TS (OG strand CDNA) 4) RNASE= rid of the RNA 5) add in the cDNA primer with the CCCC primer , add DNAP to make ds CDNA 6) Use linkers to make RE sites on the end 7) CUt with RE, put in vector, clone into host
What does MET and DNMT1 do? What does DRM (1&2) and DRM3A(3B) do? What do CMT2/3 do?
1) Maintain methylation at GC sites (keep and add on hemimethylated) 2) Put NEW methylation sites down when there is NONE to go off of. If a random gene needs silencing STILL at CG 3) Maintain and add methylation groups on CNG and CNN sites
For the " Slide 22 lecture 10 Shows a gel explaining what changes are being made at a particular promotor " explain what the 3 important bands that were seen and what they tell you about this process of histone codes and initiating transcription
1) See H4k8 acetylation at 3 hours to 8 hours first (makes sense and macthes with the enhansosome, recruiting GRN5 HAT) ALSO H3K9 is aceylated at 3hr-19 hours 2) See H3S10 phoshorylated from 3-6 hours, then H3K14 is acylated at 6-24 hours (THIS COMPLETES THE HISTONE CODE) 3) we see that TBP binds as soon as soon as H3K14 acetylates showing that H3K14 recruits TBP (
What are the types of DNA methylation?
1) Strand symmetrical 2) strand non-symmetrical
What are the 4 steps to the 5' capping (list all of the enzymes and what they do)
1) Take Phosphate away: RNA triphosphatase take off the gamma phosphate of the pre mRNA (PPP-X-P-Y....--> PP-X-P-Y....) 2) Guanyl is added on the outside= blocking guanyl: GTP comes in and with GUANYLYL TRANSFERASE to add a guanine to the end blocking the 3 PPP (GPPP-X-P-Y....) 3) RNA methyl transferase adds a methyl group onto the 7th nitrogen in the blocking guanine with ADOMET (M7G-PPP-X-P-Y...) 4) RNA methyl transferase adds ANOTHER methyl group but this time is to the next nucleotide (not the blocking guanine) (M7G-PPP-MX-P-Y...) The cap is complete 1) take away phosphate 2) add blocking guanine 3) Add Methyl 4) add methyl
What are the actual steps in splicing (do not include proteins or factors of the splicesome, just describe HOW the intron is spliced out, what attacks what)
1) The OH on the 2' Carbon on the A branch site, attacks the P group on the GU of the 5' splice site. It cuts out the upstream exon, leaving the exon with a 3'OH (NOT a P) (basically stole the phosphodiester bond) and formed a loop 2) The OH at the upsteam exon at the 3'end attacks the P group from the exon 2 and frees the lariate loop and the intron falls off
Go to slide 20 lecture 10 if needed With the IFN-B gene: what are the 5 steps (A-E) to fully activate the gene, include the enhansosome, what they recruit, when the histone code is complete Know which specific amino acids are modified during this process Know when the histone code is finished Know what this causes HOW is the initiators finally recruited and why
1) gene: with enhancer open in the promoter, but the TSS has a histone on it; ENHANSOSOME built--> ALL activators bound= enhansosome. Assemble in specific way according to the genetic code 2) recruit Histone acetyl transferase (GCN5) which acetylates H4k8 & H3k9 3) this recruits a KINASE to H3S10; and the GCN5 then acetylates H3K14 *** THIS IS THE END OF THE HISTONE CODE= What is read at the promotor in order o fully regulate 4) The acetylated H4K8 attracts SWI/SNF remodeling complex to 1) remodel the chromosome DNA or 2) displace the histone 5) The remodeled nucleosome allows TFIID (TBP) to bind because (TATA,H3K9, and H3K14 recruits it
Some nuclear receptors can act as activators or repressors depending on whether or not they are bound to their ligands. Explain the thyroid nuclear receptor >> what binds to the receptor >> what happens when TH is plentiful vs when it is absent
1. TR- thyroid hormone receptor 2. RXR - Retinoic acid receptor 3. TR-RXR dimer is bound to the thyroid hormone response element (TRE) 4. Without TH - TR-RXR recruits HDAC (histone deacetylase complex) = repression 5. With TH - TR-RXR recruits the histone acetyltransferase complex. = activation
Explain the histone code at the human IFN -B >> when do we need/start building the code? >> What does each histone modification affect in this process? >> What is it called when the transcription factors bind to the region near the promotor
>> Need code established already at/near the promoter to direct gene expression = ONLY NEEDED?ACTIVATED by viral infection >> each histone modification affects the transcription levels of nearby genes >> Cascade of events make the promoter region accessible >> FORMS THE ENHANSESOME
what are some histone marks for acetylation- what do they do, where are they what are some histone marks for methylation- what do they do? where are they?
Acetylation: H3K9, H3K14; H3K27= acetylation= activation Methylation H3K4 (M1 & M2)= activate and repress H3K4 (M3)= activate H3K9 (M2) = repress H3K27 (M3) = repress) H3K36 (M3)= activate
what does the enhansosome do?
Activator proteins bind to the nucleosome free region to further recruit remodification complexes around the TSS >> removes one specific nucleosome away from the TSS region
What is an experiment to see the timing of histone acetylation in chromatin IN humans at the IFBN promotor?
CHIP: Chromatin immunoprecipitation INVIVO EXPERIMENT
Explain the reader proteins - what they are, contain do for further regulation
COMPLEX of proteins with lots of different activities Some readers can have writer enzymes within them AFTER they read they recruit other complexes (remodeling complexes) to FURTHER regulate expression
What is one way to change chromatin structure?
Chromatin remodeling complex = 4 modes of action ****
transcription activators/factor proteins ALWAYS have 2 domains: which are the...
DNA binding domain and the Activation domain
How did they find out that the A branch point and the 3' splice site was important for splicing, what did they do and what did they see?
Did an experiment moving the A branch site and or the 3' AG splice site and saw how it affected splicing When they removed the branch site= no splicing When they moved the AG splice site= messed up splicing Helped us realize that the A branch site needed to be a certain position UPSTREAM of the 3' splice cite to have proper splicing
Regions that need to be silenced need to be maintained how it it maintained
During semiconservative replication--> proteins recognize the specific hemi-methylated site and then sends DNA methylases to methylate it
the histone code is _________ because it does not affect the base sequence of the DNA but does affect gene expression
EPIGENETIC
What is another form of EPIGENETICS? WHY
Epigenetics= not change the nt base sequence but does affect regulation of expression DNA METHYLATION: can silence or activate gene expression
The applications of CDNA are: A) Cloning the promoter region upstream of the 5' UTR of a gene B) Quantitative reverse transcriptase-PCR. for studying gene expression C) locating the positions of introns in a genomic DNA D) Expressing an ANIMAL protein in bacteria E) all of the above F) B, C, and D only
F) B, C, and D only
Coactivator and Corepressor proteins function by binding directly to the DNA and regulating gene expression T/F
FALSE they do not bind to the DNA they bind to the activators/repressors
Chromatin Immunoprecipitation (ChIP) followed by sequencing is an in-vivo method that allows for the identification of all the sites in a genome free of regulatory proteins True or false
FALSE: the whole sentence is true EXCEPT the last part. It IS an INVIVO method but tells you all the sites BOUND by regulatory proteins, not free of them
The histone code hypothesis states that gene regulation is partly dependent on histone modification that occurs ON THE DNA found in the nucleosomes True or False
FALSE: it is on the NTD of the actual histones NOT THE DNA It would be true if it was methylation of DNA
General transcription factors function to activate gene expression above the basal level: T/F
FALSE: they only do the basal level Activators go above (BZHIP, BHLH, Zinc finger)
explain where methylation has to occur to cause silencing and where it has to occur to cause activation also explain what other things are needed/present:
For silencing to occur the symmetrical ones have to be in the promoter region, ONLY IN THE PROMOTOR For activation to happen they have to be in the actual gene coding region >> also containing the other types of methylated sites upstream
The acetylation of _____ is required to recruit TBP to the promotor
H3K14
What method did they use to ID cytosine methylation at specific sites? In vivo or in vitro What do you use? Is this on a gene scale or a genome scale
IN VIVO DNA methylation experiment via restriction enzymes and southern blotting and gel - You use an isoschisomer both cut the same site 1) can not cut methylated sites, 2) one can cut specific methylated sites HPAII= no cuts; = same DNA fragment just one MSPI= 2 cuts= 3 fragments , 1 labelled THIS IS A GENE SCALE
What happens if we mutate some of the sequences in the pre-mRNA intron at the A-branch site? what happens
If the A branch point (where it actually base pairs to the U2 snRNPS) then this is bad, it can INHIBIT splicing because there is LESS complementation Remember the A in the sequence never base pairs Sometimes the RNA n the snRNP will mutate in response to the intron mutation to make binding more efficient again
Explain the steps of CHIP method- 6 main steps why its advantageous
In a living cell. Many genes have their own proteins bound to the promoter region Isolate ALL DNA with proteins attached via - Crosslinking keeps protein on DNA (formeldehyde) Then LYSE the cell fragments into many DNA pieces (this gives you all DNA with and without proteins on it) Then isolate specific protein bound to a DNA with an epitope tag + antibody bind to it ( immuno-precipitate) Isolates DNA with specific protein attached Remove the protein by reverse crosslinking Then amplify and sequence the DNA to see what is being regulated and how ADVANTAGE = IN VIVO
What does the CHIP experiment do? >> what is it similar too >> what does it allow you to do
Isolate chromatin via proteins attached to DNA >>Similar to Epitope tagging because you tag a protein with an epitope then immunoprecipitate it with an antibody, but it relies on proteins binding to their regulatory sites on DNA >> allows you to Identify ALL sites in the genome that ANY PROTEIN can bind to on DNA (tags the protein, which causes the DNA to glow too when we remove it)
What does bisulfite sequencing do?
It changes all the UNMETHYLATED C's to US so when they are fully sequenced they are turned into TS THE METHYLATED STAY AS A C
What does U5 do/recognize
It recognizes the Us in the exon 1 (3' end) and the 5' end of exon 2 and stitches them together IMPORTANT IN FORM PHOSPHODIESTER BOND BETWEEN JOINING EXONS
For the modification enzymes: What are the histone modification enzymes for phosphorylation (explain their action)
Kinases and phosphatases NOTE: OTHER MODIFICATION ENZYMES EXIST.
what does methylation do? why? What amino acid does it bind to most?
Methylation is associated with BOTH activation and repression. It only increases the bulk of the histone tails= not change the electric charge . Binds to mostly lysines
Do all of these modification processes happen sequentially? what do they interact with
NO they occur all together (AFTER the 5' cap has been put on) CO-transcriptional process ALL make contact with the CTD of the RNAP
can you clone RNA? WHat can you do?
NO you cannot clone RNA You can however make cDNA and clone that using mRNA--RTASE--> cDNA
Which of the following is true about chromatin organization at active promotors? A) contain high density of nucleosomes B) Most active promotors are free of nucleosomes C) DNA promotors are heavily methylated D) Histone H3 is methylated at K9 Explain why each may be right or wrong
NOT A) contain high density of nucleosomes = repressed YES- B) Most active promotors are free of nucleosomes= no nucleosome= free to express NOT- C) DNA promotors are heavily methylated bc methylation at the promotor= silencing NOT- D) Histone H3 is methylated at K9 histone methylation here= silencing, acylation is activation
Translation activation via a remodeling complex often involves: A) histone deacylation B) Recruiting an activator to a promotor C) DNA methylation D) Displacing the nucleosome from the promotor E) Breaking apart the nucleosome Explain why each may be right or wrong
NOT A) histone deacylation is associated is silencing NOT B) Recruiting an activator to a promotor is not via a remodeling complex NOT C) DNA methylation because usually silencing YES- D) Displacing the nucleosome from the promotor NOT E) Breaking apart the nucleosome because its not a thing
What is a basic subunit of chromatin?
NUCLEOSOME (histone protein plus 146 bp of wrapped DNA)
What is a northern blot? > how do you know if you have more or less expression >> what kinds of things can it tell you
Northern blot is an extension of Southern blot that uses RNA instead of DNA for testing. Analyzes RNA fragments (mRNA) on a gel electrophoresis using a probe Thicker bands show more expression use hybridizable probe, more probe seen= more transcripts in the well BIG | | Small Can tell you relatively HOW much transcription At what stages in development and compared to where in the body (this is hard bc lots treatment groups)
what does northern blot give you in terms of gene expression vs a run on assay? HOW would these 2 look on a graph if you 1) measured 2 different genes, who had the SAME run on assay but then looked at them on a 2) northern blot
Northern blot: transcriptional abundance= NET abundance (synthesis- degradation) Run on assay= JUST synthesis rate , no degradation IF you took 2 seperate genes and they had 1) THE same transcriptional rate, their blot paper will be the same but when you 2) graph them via northern blot they will have different levels of degradation and the overall net will not be the same
what does phosphorylation do? why? What amino acid does it bind to most?
Phosphorylation is associated with activation this is because it makes the end of the histone tail negative; she said "neutralizing the charge" NOW the DNA and histone are not tightly bound= can free out the histone and then activate transcription Serine, Threonine, Tyrosine
Compare and contrast transcription of prokaryotes vs eukaryotes
Prokaryotic: Transcription and translation are coupled all happening in the cytoplasm Eukaryotes: transcription of mRNA, Processing, and splicing in the nucleus, carried out to the cytoplasm to translate Prokaryote: we understand transcriptional termination (specific site with a hairpin immediately translated Euk: we do ot know the termination. they have to go under several modifications and processing steps before exporting to the cytoplasm (MRNA cap, 3' poly A tail and splicing) then it can be translated. Modifications turn pre-mRNA to mature mRNA
What is a Run on assay? What does it measure how do you do it
Quantify/measure transcription (INITIATION) counting ALL the mRNA in the cell being made. Does not include the net amount after degradation. JUST SYNTHESIS YOu take all the nuclei out of he cell put it in a culture tube . it will not make mRNA unless you put labelled 32-P-NTPS. when these P-NTPS are added, they allow all the mRNA to glow = ALL mRNA in this cell is being labelled If want to measure a specific genes rate= extract with a probe on northern blot Tells you synthesis rate. The deeper the color the more the transcriptional synthesis
Explain the model for polyadenylation of the 3' end
RNAP goes along making the mRNA, passes the consensus sequence for the poly A (AAUAAA) then reaches the GU or U rich region it recognizes these regions and recruits multiple proteins and complexes in order to fully cut it off and start the adenylation process
REMINDER:
Reader/Writer complexes can spread along + Remodeling complex + methylation complexes all at once
How can we identify methylation sites of a larger genome scale?
Sequence the entire genome Identify the sites by BYSULFITE sequencing 2 groups 1) regular sequencing vs 2) bisulfite sequencing
In humans and in plants what is the sites for symmetrical methylation NON -symmetrical?
Symmetrical: HUMANS = (m)CG Plants ALSO CG, but also CNG NON symmetrical: plants CNN
Give the ingredients of sybr and Taq man what are the 4 steps of each
TAQMAN: 1) Need a probe that matches a single DNA >> forward and reverse primer >> DNTPS and DNAP : only makes a glowing color when the probe is broken up by DNA SYBR: Need Primers (regular) , DNTPS, DNAP, and a DYE SEE amplify in real time 1) cDNA denature 2) Dye/Probe bind to DNA 3) Flouresence signal detected 4) Flourescence increase with more synthesized dna in REAL TIME
How do the major transcriptional regulators and chromatin regulators work in terms of the overall process?
THe activators, nucleosome remodeling complex, histone modifiers all work together to increase gene expression, not on their own
RNAS that are polyadenylated, spliced, and capped are MOST efficiently transported out of the nucleus for translation T/F
TRUE Guide out of nucleus protect from degradation in and out of the nucleus allows proper proteins to be made
Explain what is methylated: and what umbrella term enzyme is used to do this Regions highly methylated= ______ _______
The 5th carbon of the cytosine is methylated DNA METHYLTRANSFERASES Regions highly methylated= highly compact = gene is usually silenced
What is the histone code?
The histone code refers to modifications to the tails of histone proteins. These modifications include the addition or removal of phosphate groups, acetyl groups, or methyl groups. As a consequence of these modifications, pattern of gene expression changes. COVALENT MODIFICATIONS OF CORE HISTONE TAILS
how does the snRNP interact with the intron (pre-mRNA) it is splicing?
The snRNP is composed of proteins that catalyze the reaction but they are also composed of RNA that hybridize to the intron and they bind to do their work
What is a histone mark? What does acetylation usually do? WHY- >> what amino acids does acetylation target
The specific and singled out described form of the histone modification Acetylation usually does activation of transcription - The acetyl group reduces the + charge of the N terminal group. of the histone This weakens the binding of the histone to the DNA= more accessible -Usually targets lysine amino acids
How do we know where to cut the DNA off to poly adenylate it?
There are 2 major sequences needed to cut off the DNA and allow polyadenylation 1) There is a consensus sequence first "AAUAAA" which has 98% consensus so its super efficient 2) The consensus sequence is followed by a GU or U rich region 20-30 bp later. NEEDS BOTH OF THESE TO GET CUT OUT
In terms of splicing mRNA: HOW does the cell know where introns are and where to splice? Why is splicing necessary
There are 3 specific sites in the actual mRNA sequence NEEDED to splice: the 5' end of the INTRON= GU the 3' end of the INTRON= AG the middle of INTRON= "A" branch site (does actual splicing) proteins come and assist by binding to these sites The 3' end of the 1st exon and the 5'end of the 2nd exon are also important because U5 will help them bind to each other but that will be discussed later
Explain the splicesome proteins (snRPS) (all of them) what each does what ones are the most important?
U1: Recognizes the 5'splice site 1st (GU) which is then replaced by U6 U2: Recognizes the A branch point U2AF: Recognizes the Pyrimidines in the branch point, mostly recognizes the 3' splice site U5: recognizes the 5' and 3' splice sites of the introns, then stitches together the 3' end of exon 1 and then the 5' end of exon 2 to each other. U6: recognizes the 5' GU splice site Most important= U6 U5 U2
HOW do modifications happen on the histone tail and how are they recognized (what is the overall process of their markings- what proteins and or complexes are associated with each step
Write--> read--> remove 1) writer proteins (HAT, HMT, PRMT) write the modification mark that can change the chromatin state 2) the reader protein complexes read the mark to recruit proteins for gene expression/repression= actual regulation (Bromodomain, Chromodomain) 3) Erasers remove the mark (HDAC, KDM)
Which statement describes the relationship between METHYLATION and gene activity ? A_ DNA methylation is usually associated with transcriptional Inactivity B_ DNA methylation is usually associated with translational inactivity C_ DNA methylation is usually associated with transcriptional activity D_ Histone methylation is usually associated with transcriptional inactivity E_ Histone methylation is usually associated with transcriptional activity Explain why each is right or wrong
YES---- A_ DNA methylation is usually associated with transcriptional Inactivity NO----- B_ DNA methylation is usually associated with translational inactivity NO---- C_ DNA methylation is usually associated with transcriptional activity --NO---- D_ Histone methylation is usually associated with transcriptional inactivity -NO----- E_ Histone methylation is usually associated with transcriptional activity
Think of an experiment that will show how the capping enzyme, splicesome, and poly A complex binds to different regions of the mRNA
You could do an RNASE footprinting assay to see what regions are protected when you add pre-mRNA with the cap and different proteins YOU could also do a gel-shift assay OR a RIP (like a chip but with RNA)
what does a reporter gene assay do?
You fuse the promoter of interest (interested in seeing gene expression) to a eporter gene like beta galactosidase this way, you can physically see WHERE it is being made and HOW MUCH by how dark it gets Can use this in different developmental stages , see blue color at different times see which genes are important for expression. and see where transcription starts
What is a nuclear receptor?
hormone binding allows the receptor to regulate the expression of specific genes
What is a spliceosome? What is it made out of?
protein complex for splicing INCLUDES : pre-mRNA + Proteins+ RNA RNAS and proteins SOME Proteins are coupled with RNA = snRPS (small nuclear RNAS) and do the bulk of the work
Slide 22 lecture 10 Shows a gel explaining what changes are being made at a particular promotor : Did an CHIP and isolated every hour, looked on a gel, see what histones or proteins are present at what time --> what does this tell us
tells us what histone marks are made first and what completes the histone code before TBP can bind to the promotor
What is 5' capping? >> when does the cap get put on?
the addition of 7-methyl guanosine to the 5' end of pre-mRNA >> while transcription has begun and is still continuing the cap is put on when 20-30 nt have been made
Why does splicing need to be regulated?
to create diversity of proteins you need called alternative splicing 25k genes but 100k proteins MANY things trigger alternative splicing
HOW can you measure expression of mRNA via cDNA ?
via RT-PCR (real time q PCR) Isolate specific RNA make CDNA 00> amplify with a specific quantitative ingredient 1) PROBES: TaqMAN 2) DYE= SYBR
What is polyadenylation? what are the 3 main general steps (DO NOT add enzymes)
when a 3' poly A tail is added to the pre-mRNA A) There is a polyadenylation site near the 3' end of the pre-mRNA which ALLOWS the 3' end to be cut off (gets cut off) (5' ---------\-----3'. --> 5----------\. -------) B) Polyadenylation: 50-250 adenines are added to the end C) Degradation of the 3' end that was cut out earlier
what happens when you modify the histone tails? What is it called overall when we add a functional group onto their histone protein tails? what type of modifications are there, and is it random?
when the N terminal histone tails are modified, they direct processes depending on where they are protein modification post translational the modifications are Methylation, acetylation and phosphorylation and NO they are not random. They are specific to specific amino acids and direct specific processes