Lecture 24: Amino Acid Biosynthesis Flashcards

1
Q

what does glyphosate inhibit?

A

the Shikimate Pathway

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2
Q

How many amino acids do humans make?

A

about half
those are nonessential

the essential amino acids are those we cant make and have to get from our diet

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3
Q

arginine

A

essential amino acid
needed in diet for rapid growth in childhood and pregnancy
BUT it IS MADE in the urea cycle

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4
Q

tyrosine

A

conditionally nonessential: it is made in humans from essential amino acid phenylaline.
so we need to get phenyaline in diet in order to make tyrosine

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5
Q

where do carbon backbones of most amino acids come from?

A

metabolites from glycolysis, pentose phosphate pathway, and citrate cycle

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6
Q

how many steps to make nonessential vs. essential amino aicds

A

very few for nonessential 1-2 steps
like 10 steps for essential

so humans just make nonessential
bacteria and plants make all

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7
Q

what can many amino acids be made from?

A

OAA and pyruvate: make carbon backbones
nitrogen components come from gultamate and are put on by aminotransferases

OAA and pyruvate parts linked

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8
Q

what class of amino acids are phenylaline, tyrosine, and tryptophan

A

aromatic
made by shikimate pathway
round up heracide targets shikimate pathway

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9
Q

what is the thing used in roundup? what does it do?

A

glyphosate
it inhibits enzyme EPSP synthase
which is need for making phenylaline, tyrosine, and tryptophan

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10
Q

do you think glyphosate works faster in summer and winter? why?

A

summer

because there is more active growth in the summer, and so they need amino acids bad

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11
Q

why do we use roundup?

A

animals don’t have the shikimate pathway, so it doesn’t harm them

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12
Q

what about for crops we don’t want to kill? how does rounup work then/

A

they engineered glyphosate resistant crop plants and sprayed with round up
they can still grow, but weeds are killed

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13
Q

concerns with GMOs

A

expensive
we don’t know if they’re safe yet
may be other ways to adressess food needs
ecological concerns: can the genes spread to other plants and beyond our control?

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14
Q

why are amino acids used to make a lot of other things

A

because they all have nitrogen and most are nitrogen rich

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15
Q

what are some things made by amino acids

A

heme groups
nucleotide bases
signaling molecules

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16
Q

example of amino acid as metabolic precursor: Tyrosine

A

converted into dopamine
dopamine can go to epi, norepi

important in production of melanins (metabolized by tyrosinase)

17
Q

2 types of melanins

A

eumelanins: dark pigments
pheomelanins: light pigments

18
Q

Loss of pigment

A

with age, melanin production shuts down

melanocytes not replaced when they die at this point

19
Q

Phenylketonuria: PKU

A

defect in amino acid metabolism: we can’t get tyrosine from phenyalanine b/c phenylalanine hydroxylase doesn’t work

pretty common

if untreated: severe mental retardation, stunted growth, dental problems
so screen in infants

20
Q

More on PKU: why is too much phenyaline bad?

A

accumulation of phenylalanine means it gets made into toxic metabolites

ITS NOT BECAUSE WE LACK TYROSINE!!!!!
its because of accumulation of toxic metabolites made instead

treatment: don’t eat much phenylalanine: its in NutraSweet, which is in lots of of proccessed foods with aspartame

21
Q

Showing symptoms of PKU

A

you have to inherit two defective copies: mom and dad both have to be carriers
in this case: 25% chance of offspring having PKU

22
Q

What is the probability of having a PKU child of mothers genotype is Pp and fathers is Pp (both carriers)?

A

25%

23
Q

What is the probability of having a PKU carrier child if mothers genotype is PP and fathers is pp?

A

100% 1 copy from mom, 1 from dad = Pp

24
Q

Albinism (type 1) caused by…

A

defect in tyrosinase gene

don’t synth pigments b/c of lack of this gene

25
Q

how is albinism different from PKU?

A

symptoms of PKU caused by buildup of toxic metabolites

symptoms of albinism due to LACK OF REACTION PRODUCTS not accumulation

26
Q

Would someone w/ PKU have light skin and hair?

A

yes at birth b/c of low tyrosine levles

BUT they darken because of dietary tyrosine

27
Q

Congenital porphoryias

A

affect heme biosynth
they’re involved in making porphyrin ring that makes heme
lots of steps, lots of room for issues in this pathway
can be result of dominant mutations

28
Q

dominant mutations

A

cause symptoms when only one defective gene is inherited b/c encoded protein has new “bad” function

29
Q

Acute intermitent porphyria

A

dominant mutation in porphobilinogen deaminase gene

variable symptoms
abdominal pain, motor weakness, urinary symptoms, tingling and numbness in fingers, hypertension, sweatyness, autonomic nervous symptoms, electrolyte abnormalities

offspring would have it too

30
Q

Congenital erythropoietic porphyria

A

recessive diease causing accumulation in heme precursors

red urine, reddish floruscent teeth, sensitive to sunlight, anemic