- Hey, y'all my name is Prashanth Kumar, or PK,
and I'm an MCAT tutor at Shemmassian Academic Consulting.
Today, we're gonna be doing five questions
from the MCAT Bio/Biochem section.
Specifically, the discrete questions.
Should be taking roughly a minute and a half
for each of these questions,
but today we're gonna be going more in depth
so you can see exactly what's going on in my head
as I tackle each of these questions.
Let's get it.
(typing sounds)
All right,
Before we get started, make sure to like the video
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With that, let's get right into these five questions.
So, I've gone ahead and put them right here
but I'm gonna go through it and zoom in
so you guys get a better look at each of the questions.
And so, with that,
feel free to take a moment, pause the video,
go at it at your own pace,
and come back to us.
If not, let's get right into question number one.
For me, I like to think of the discrete questions
as a blessing.
It's really nice to not have to read a passage once again,
and they're a nice respite after these long,
oftentimes boring passages.
And so, I like to think,
so these are the ones
that we're really gonna wanna finish quickly, okay?
So, the reason is, we don't have to read a passage.
If we only have to read a question,
it should be question, answer, almost immediately.
Or, a little bit of calculation
and get the answer immediately.
So, think of this as a faster paced question,
maybe a minute to a minute and a half
for each of these.
But, with that,
we can get right into question number one.
Researchers are studying a potential novel oncoprotein
implicated in gastric cancer, RT-qPCR
results show an upregulation
of the mRNA transcripts of the novel protein.
Which of the following is a potential mechanism
by which transcription of the protein is upregulated?
Is it A, opening of chromatin structure,
B, histone deacetylation,
C, increased ribosome synthesis
or D, increased amino acid availability.
All right.
So, the nice thing about these sort of discrete questions
is that the question is the only thing
we really need to focus on.
We can read through it just to understand the details,
sometimes they might ask,
but for the most part,
the question is really the only thing we care about.
So here, the question is
mechanism for transcription
of the protein being upregulated.
Something simple,
and we're just looking for an answer choice
that will allow us to choose this.
So, right away, we're looking for something
that increases transcription rates.
And so, that requires an understanding
of what does transcription do.
Transcription, I'll just call it TC,
just so we don't get confused.
That is the process of turning DNA into RNA, big picture.
And then what is the counter of it?
It's translation.
It's the second step and that is turning RNA to protein.
And so this question is specifically asking
about transcription, not translation.
So anything dealing with DNA to RNA, we can focus on
but anything with RNA to protein
we don't really care about.
And so right away we see two or choices we can eliminate
because they're dealing with proteins and that's C and D.
We don't really care about ribosomes or amino acids
because those are associated with protein creation.
So right away, we're at a 50/50
or we know it's down to A and B.
So we should know
that the way we increase transcription
is we want more access to the DNA.
That's the idea,
increase access to the DNA
results in increased transcription.
Okay, so there is an answer
that looks pretty good right away.
And that's A, opening of chromatin structure
is how we have more access to the DNA.
And so the way we do this
is by these biological modifications
of the acetylation and methylation.
And so I am going to move this a little bit up.
I'm gonna move this.
I'm gonna erase this for now.
And so the reason I wanna focus
on this is because this is a very important idea
this idea of acetylation and methylation.
And then I'm also put a dash here
then I'll put D here and you'll see why in a second.
So the reason is I wanna say
if we have normal acetylation,
that means we're gonna have increased transcription rates.
Transcription.
Whereas if we have methylation of our DNA,
we're gonna have decreased transcription rates.
And so if we are dealing with deacetylation,
we're gonna have decreased transcription rates.
Whereas if we have demethylation,
we're gonna have increased transcription rates.
And so this sort of like table I created very loosely
is exactly what we're thinking about
when we're dealing with transcription.
Remember we're looking
for something that will increase transcription rates
by increasing access.
And that would be in this case
acetylation right here, or demethylation,
not deacetylation
So you can eliminate B and we're left with A,
increase access to the DNA
whether it's through acetylation
or demethylation is the same idea of opening
up the chromatin structure for more transcription to occur.
And with that, we're one for one,
right onto question number two.
A red flower is mated with a white flower,
resulting in pink progeny.
This is an example of A, co-dominance,
B, heterodominance,
C, complete dominance
or D, incomplete dominance.
So a genetics question,
dealing with types of heritability.
Right away, we should know these types
of heritability off the top of our head,
very, very strongly.
So co-dominance, is this idea
of both properties
of the parents being assertively dominated together,
it's gonna be equally dominant in this situation.
So the idea I always look at,
is we have a pink flower,
And I'll actually do it with the colors this time.
So we have this like red flower
and then we have a flower with black dots on it.
And so when we put them together,
we're gonna result in, I'll draw them.
We're gonna have a red flower with black dots.
So we're gonna see both traits
equally expressed in this
and they're able to sort of cooperate together.
Whereas hetero dominance is a made up term.
It's not something we learned.
So we're gonna get rid of that.
Complete dominance is, okay,
we have this red,
or I'm gonna draw this arrow right here.
And so we have this red
or in this black flower, for example.
Only one of them will be able to be the more dominant one
if they both are paired together.
And so you're usually gonna see the red flower
75% of the time.
And then you could also see the black dotted flower,
25% of the time.
So this is assuming the red is the dominant,
the black is the recessive.
And so with that, we'd see a mix of both of them
if we saw a bunch of them.
So now incomplete dominance is this exact situation
that we're looking for.
I'll draw it in green, down here.
Incomplete dominance says, okay,
let's start with a red flower and a white flower.
We're gonna blend, I guess you can't see the white
but we're gonna blend these to make,
that's a better pink.
We're gonna make a pink flower out of both of them.
That's the common example we see.
It's a blend somewhere in between 50% of
the red and the white, pink.
And so incomplete dominance is what we're gonna pick
as our answer choice, not complete dominance
and not co-dominance.
People oftentimes get confused
between co-dominance and incomplete dominance.
I like to think co-dominance is a situation
where both qualities are not moderated at all.
They're put together and it's like bit a big mess together.
Whereas incomplete dominance is like kind of the moderator,
you're like in the middle of both qualities
whereas you're not strongly biased to either,
whereas co-dominance,
you're kind of polarized and biased to both.
Question number three,
a non-diabetic individual
eats a large carbohydrate risk rich meal,
which of the following glycolysis enzymes is insulin
most likely to upregulate?
Is it A, phosphoglucose isomerase,
B phosphofructokinase-1,
C phosphoglyceromutase,
D, Enolase.
So the idea is we're just looking after a big meal, eating,
which of the following glycolysis enzymes
is insulin most likely to upregulate.
So we know insulin causes an increase in glycolysis.
We eat more food.
We wanna turn that into energy.
So we're gonna have increased glycolysis.
And so the important part of this discrete question
is not knowing necessarily each the steps of glycolysis
but really one important detail.
And that is the rate limiting step.
The rate limiting step is the step usually targeted
by hormones or enzymes.
And this is the step
for which you increase or decrease the rates of something,
that step is always targeted.
And so in this case
we need to know the rate limiting step of glycolysis.
And if there's one sort of enzyme
I want you to know it is phosphofructokinase.
That's probably the most, most, most important one,
especially for glycolysis.
And that is the rate limiting step for glycolysis.
And so this will be the step that is regulated
the flow through glycolysis by insulin.
So insulin will target glycolysis right in pink,
via PFK-1.
The other enzymes, not really important
They're, they're part of the steps
but they're not the steps that are being regulated
very, very heavily.
They're not the rate limiting step.
The rate limiting step is the step
which is able to be monitored very, very heavily.
All right, onward to question number three.
Eliminate A, C and D for that reason.
Onward to question number four.
Cells are treated
with a drug that dissipates the proton gradient
across the inner mitochondrial membrane.
What is the net result?
A, cancer progression is halted.
B, ATP cannot be produced via ATP Syntase,
C, the cell will use exocytosis
to dispose of the nonfunctional mitochondria
or D, cells will rapidly evolve
a new ATP synthesis mechanism.
All right, so the idea is that
we're dissipating proton gradient.
These should be buzzwords that you're hearing
in your head over and over again
right across the inner mitochondrial membrane.
What is the net result?
So we want to think
what is this inner mitochondrial membrane
and what does it do?
So when we're thinking mitochondria,
powerhouse of the cell,
what is it doing?
It's related to protons and ATP Synthase.
As we're creating ATP,
is due to this proton gradient.
So I'm right away thinking, huh?
Proton gradient ATP.
So if we're dissipating the proton gradient
then we're gonna have less ATP available.
So I'm gonna eliminate A and C almost immediately
because they don't have anything to do
with proton gradients or ATP.
And so we're down to B and D,
ATP cannot be produced via ATP synthase,
or D cells will rapidly evolve
a new ATP synthesis mechanism.
Right away, without even thinking
about ATP synthase too much,
we should know that cells won't be able to adapt
that quickly.
If we just say here's a drug.
They're not gonna create a new system
of ATP synthesis right away,
rather they're gonna rely on glycolysis probably
without the mitochondria.
And so we can eliminate D,
because there's no new thing gonna be evolved
almost immediately.
It takes time, decades, centuries, all of that.
And so B is right away, our big and best answer,
but let's just make sure we understand this.
So we have our sort of membrane.
I'm gonna draw that as the inner membrane.
And so as we go through our sub units, our H pluses
are going across the membrane.
And so the whole point of the mitochondria
is that when we're going from this matrix
to this inner membrane space,
we're just pumping out these protons
into the inner membrane space from the matrix
or other way around
into the matrix from the inner membrane space.
And so the whole point is
it's generated for this thing called ATP Synthase,
where we have a bunch of H pluses
and then the H pluses will build up on this side
and pump back in to reach
ADP and turn it into ATP.
So this is the big picture idea.
So that protons flow
from the inner membrane space into the matrix.
So I'll write this out,
enter
brain space
matrix.
So protons will pump out into the inner membrane space
and then flow back in through ATP syntase
to create ATP via ATP Synthase.
Sorry if I confuse you, it's starting from the matrix
pumping out to the inner membrane space, pumping back in.
And so this is the big picture idea
of why we're creating that proton gradient.
So all of a sudden, if we have a drug that dissipates that
then there's not gonna be enough
in the inner membrane space to pump back in
to the matrix or to create ATP.
All right, with that, let's go
onto our final question of today, five.
Following a viral infection,
a patient does not show any respiratory symptoms or fever.
What cycle is the virus most likely in?
Is it A, Lytic,
B, Lysogenic,
C invasion or D protein production.
All right, right away, we should note
that C and D are not types of viral cycles
that we've heard of.
The two main ones we've heard of
are the lytic and the lysogenic cycle.
And so the two things I want you to remember is
lytic is more of the destroy immediately type of thing
And lysogenic is playing the long game.
And so if you're playing the long game,
you want to ingrain yourself in the cell's DNA
and then allow yourself to multiply
for longer, longer time until something stressful happens.
And the cell goes haywire.
So I'll illustrate it in two ways.
So first we'll start with the lysogenic cycle.
This is a long game.
And so a virus,
I'll draw it with a green spiky,
attacks a cell,
and I'm gonna draw a red little DNA, so get the DNA in it.
And so what happens is that this green
joins into the red just here.
All right, question number five,
following a viral infection,
a patient is not showing any respiratory symptoms or fever.
What cycle is the virus most likely in?
Is it A, lytic,
B, lysogenic,
C invasion or D protein production.
All right, so the question is asking us pretty simply
what cycle is this describing symptom.
And so we're looking for a virus cycle.
That's the first thing.
And so right away, we can eliminate C and D
because these aren't cycles that we've heard of before,
we're not gonna waste time on them.
These are discrete questions.
They should be quicker.
So right away it eliminates C and D,
and we're down lytic and lysogenic,
the two most common viral cycle that we've learned about.
So a lytic cycle, I like to think about
is sort of the fast break everything.
And the lysogenic is sort of playing the long game.
And so those are my two sort of descriptive factors.
And with that we should be able to pick
B almost immediately,
but let's go through it.
Let's go make sure we understand the lytic and lysogenic.
The lytic cycle is the virus comes in
and sort of starts destroying the cell,
lyces the cell.
Lytic comes from lyce.
So lyce the cell, break it up,
break up and then it likes to remake itself,
remake virus progeny.
And that's very, very important.
It's taking the cell, breaking it up
and using the little bits and pieces
and salvage and making more and more of itself.
And so that's how it multiplies.
The lysogenic is playing the long game.
And so it's going to ingrain itself in host DNA,
allow the cell to multiply normally
and then break cell with stress.
So the idea is that sneakily just attaches itself
to the host DNA
and the host thinks it's part of the normal DNA.
So it's gonna replicate, replicate, replicate
with more and more cells.
And all of a sudden we're gonna have some sort of stress.
Some sort of stress from environment,
from whatever that'll just cause everything to be chaos.
All the cells are gonna have that like code
to say all right, time to break.
And so that's exactly what it is.
It's an immediate sort of breakdown
and a lytic cycle versus a longer term,
okay, let's play the long game,
multiply, multiply, multiply snap,
all of the sudden, bigger casualties in the longer term.
And so with that, we see that the patient
is not showing any respiratory symptoms or fever.
Nothing's happening right now.
So we're not expected to see
the break everything,
everything's broken right now.
More we're focused on the long game.
The virus is building it's army.
It's getting ready to attack.
It doesn't need to attack yet.
All right y'all,
we crushed five questions right there.
Super, super helpful discrete questions,
running everything from DNA modifications to genetics,
to ATP all of that.
So great job getting it done.
Super, super challenging questions.
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