Lecture 24: Amino Acid Biosynthesis Flashcards
what does glyphosate inhibit?
the Shikimate Pathway
How many amino acids do humans make?
about half
those are nonessential
the essential amino acids are those we cant make and have to get from our diet
arginine
essential amino acid
needed in diet for rapid growth in childhood and pregnancy
BUT it IS MADE in the urea cycle
tyrosine
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
where do carbon backbones of most amino acids come from?
metabolites from glycolysis, pentose phosphate pathway, and citrate cycle
how many steps to make nonessential vs. essential amino aicds
very few for nonessential 1-2 steps
like 10 steps for essential
so humans just make nonessential
bacteria and plants make all
what can many amino acids be made from?
OAA and pyruvate: make carbon backbones
nitrogen components come from gultamate and are put on by aminotransferases
OAA and pyruvate parts linked
what class of amino acids are phenylaline, tyrosine, and tryptophan
aromatic
made by shikimate pathway
round up heracide targets shikimate pathway
what is the thing used in roundup? what does it do?
glyphosate
it inhibits enzyme EPSP synthase
which is need for making phenylaline, tyrosine, and tryptophan
do you think glyphosate works faster in summer and winter? why?
summer
because there is more active growth in the summer, and so they need amino acids bad
why do we use roundup?
animals don’t have the shikimate pathway, so it doesn’t harm them
what about for crops we don’t want to kill? how does rounup work then/
they engineered glyphosate resistant crop plants and sprayed with round up
they can still grow, but weeds are killed
concerns with GMOs
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?
why are amino acids used to make a lot of other things
because they all have nitrogen and most are nitrogen rich
what are some things made by amino acids
heme groups
nucleotide bases
signaling molecules
example of amino acid as metabolic precursor: Tyrosine
converted into dopamine
dopamine can go to epi, norepi
important in production of melanins (metabolized by tyrosinase)
2 types of melanins
eumelanins: dark pigments
pheomelanins: light pigments
Loss of pigment
with age, melanin production shuts down
melanocytes not replaced when they die at this point
Phenylketonuria: PKU
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
More on PKU: why is too much phenyaline bad?
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
Showing symptoms of PKU
you have to inherit two defective copies: mom and dad both have to be carriers
in this case: 25% chance of offspring having PKU
What is the probability of having a PKU child of mothers genotype is Pp and fathers is Pp (both carriers)?
25%
What is the probability of having a PKU carrier child if mothers genotype is PP and fathers is pp?
100% 1 copy from mom, 1 from dad = Pp
Albinism (type 1) caused by…
defect in tyrosinase gene
don’t synth pigments b/c of lack of this gene
how is albinism different from PKU?
symptoms of PKU caused by buildup of toxic metabolites
symptoms of albinism due to LACK OF REACTION PRODUCTS not accumulation
Would someone w/ PKU have light skin and hair?
yes at birth b/c of low tyrosine levles
BUT they darken because of dietary tyrosine
Congenital porphoryias
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
dominant mutations
cause symptoms when only one defective gene is inherited b/c encoded protein has new “bad” function
Acute intermitent porphyria
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
Congenital erythropoietic porphyria
recessive diease causing accumulation in heme precursors
red urine, reddish floruscent teeth, sensitive to sunlight, anemic
