Class Notes (1,100,000)
CA (630,000)
UTSC (30,000)
BIOB11H3 (300)
Dan Riggs (200)

BIOB11H3 Lecture Notes - Iron Response Element, Histone Acetyltransferase, Cpeb

Biological Sciences
Course Code
Dan Riggs

This preview shows pages 1-3. to view the full 11 pages of the document.
Lec 11
Transcription factors have both dna binding and activation. They have binding
domain and transcription factors that can turn on genes or repress it.
So one allows for it to bind for the right sequence and one affects its function.
In the major groove of the helix scructure allows for nucleic acids to be more easily
Within that major groove, the nitrogenous bases are easily accessible.
Many different classes of transcription factor:
Major ones: zinc finger TF will form a loop facing the major groove.
The helix loop helix transcription factor bind as dimers, usually in the form as
Leucine is a hydrophobic side chain. Leucine is found on every 7th amino acid.
The leucine motif is to zip up.. the interaction between the molecule is to shield
themselves from the water.
This motif is used in the bZIP factor.
B domain Is the basic domain. It mediates the specificity of DNA binding.
For microarray, you get a robot that samples all genes. Another robot uses a printing
process to print spots on a solid surface.
The grid or chip generated has specific sequences in specific grid positions.
The detection and quantitation is based on the fluorescent labeled cDNA that
hybridizes to the grid spots. It is a hybridizing technique.
If there’s microarray sites where they will complement both red and green cDNA,
you’ll get a yellow site.
In a red spot, beta galtosidase expressed when lactose is present and if green, it
means it’s absent.
If yellow, it means beta galactosidase is rexpressed under both conditions.
Microarray can be used to find which genes are regulated by transcription factors.
In a mutant, no transcription factor and if the transcription factor activates that
gene, then no target transcription take place.

Only pages 1-3 are available for preview. Some parts have been intentionally blurred.

Up list are genes that are up regulated in the mutant, they are expressed at a higher
level in the mutant. In the wildtype, transcription factor negatively regulates them.
So when they’re not present, theyre knocked up?
Lec 12 - Gene regulation
Epigenetics alter gene expression but don’t change te sequence of DNA.
The histones that package that DNA are often modified. Often what happens is a
methyl group gets added to the histone or dna (or removed).
Most of the cell cycle, chromatin is a decondensed state like a bowl of spaghetti.
Other times, it is incredibly condensed like a bread stick.
Most of the time the chromatin in the decondensed state, is called interphase.
Mitosis the time of segregation of the condensed chromosomes go on.
They have to go to the condensed, silent state to an active decondensed state.
Most of the dna from daughter cell is labeled as euchromatin which means it returns
to dispersed reconfiguration state after mitosis.
Some of the chromatin remain condensed is known as the heterochromatin.
=constitutive (means always) heterochromatin. Some fraction of the chromosome
remains condensed no matter what. E.g. repetitive dna of the centromeres.
=faculatative heterochromatin remains condensed depending on the cell stage. E.g. x
chromasomes in females.
Human females have 2 x chromosomes. And males got one x chromsosome from
mom and one y from dad.
But females really only one active gene.
=one of the two x chromosome in every cell will be randomly inactivated.
The calico cat has a mosaic of fur type. Coat color controlled by several genes. One
controlled by the x chromosome will be for black. The other for orange coat.
=random activation during activation, will cause some regions that are black and
some are orange.
XIST gene is a very large gene that encodes a very large non-coding RNA, meaning it
wont transcribe to protein. There are many copies of it and will encode the entire
Methyl dna will come in and shut down one of the x chromosome.
In fig 12-14, the Ac are the groups that added, sometimes lysine, serine, etc.
The n terminus tail of H3, you can see large letters of A and R, which is for activating
or repressing.
12-17, heterochromatinization packaging of chromatin into a very tight structure.
Dicer wil cut the rna into pieces.
=the guide strand is coming with a protein complex to a place where it needs to be
=as rna is rolling off, there’s a sequence complex that is being produced.
=suv39h1 is a histone methyl transferase. It transfers methyl groups to some of the
histone molecules.
K=one letter code for LYS.
H3 is for histone 3.

Only pages 1-3 are available for preview. Some parts have been intentionally blurred.

The boundary element serves as a stop sign for heterochromatin to stop at this
point. It is to keep adjacent genes to be condensed, so they don’t become
transcriptionally active.
Hormones are key regulated of gene expression.
Cortisol is escorted into the cytoplasm and interact with soluble receptors.
This will translocate to the nucleus. Then you’ll prevent certain gene activations.
The steroids induce or repress the expression of genes. E.g. transport processes or
growth home, etc.
Glucocorticoid receptor binds to the GRE- glucocorticoid response element. So when
GR binds to GRE,
CPB is a histone acetyltransferase. It transfers acetyl groups to certain histone
Note: tata box seems to be tightly wounded, so it’s not readily accessible. So the goal
is to loosen the nucleus from the tata box to be revealed to ttb?
Once CBP acetyls histones, it changes.
SWI/SNF is a chromatin remodeling complex.
General transcription factors will then bind when TATA box is revealed.
The steroid binds receptor, finds cis sequence, events happen to open chromatin to
allow RNA polymerase assemble and eventually allow transcription(?)
fig 12-49. You acertylate to make things active. So HDAC takes off the acetyl group.
=to prevent this from reversing, methylation of formerly acetyl histones will be in a
tight states, denying polymeraization and transcription is essentially shut off.
=so methyl group is the seal to put it into a tight state to deter access.
Chromatin regulators will come in and facilitate the loop?
Alternative splicing is to make multiple mrna from the same type of transcript.
Imagine you have a heterogeneous rna.
E3B E3A are exons highlighted in blue. In some cases, in say a tissue of fibroblast,
exons need to be present in all mRNA.
In other cells, 2 exons must be spliced out so that we get a somewhat different mRna
like a liver mrna.
In order for splicing to take place. Splicsome must make specific cuts and then put
the introns back together. Snrps, etc, have to be attracted to splice sites. They are
attracted to the splice sites due to regions of splicing enhancers (as well as
If spliceosome is not recruited, exon 2 will be removed with the adjacent exons.
When fertilization takes place, it is associated with CPEB phosphorrylation.
You're Reading a Preview

Unlock to view full version