Fa Biochemistry-Molecular High-Yield Facts And Mnemonics

Front 1

How many histones are in a nucleosome? What are they? Which histone is not included in the nucleosome?

Back 1

There are 8 histones in a nucleosome; 2 of each H2A, H2B, H3, and H4. The H1 histone is a linker histone and is not part of the nucleosome.

Front 2

What role does acetylation and methylation of histones play in DNA expression?

Back 2

Acetylation is a negatively charged group added to histones. This decreases the DNA affinity for the histones and allows for increase transcription.

Methylation works in the complete opposite manner and represses gene expression.

Front 3

What is the difference between a base, nucleotide, and nucleoside?

Back 3

The base consists of merely the purine or pyrimidine. NucleoSides have the Sugar attached to the base while the nucleoTide is a nucleoside with a phosphaTe attached.

Front 4

What are the main purines and pyrimidines? Which are single ring structures? Double ring?

G typically bind C and A binds T...which bond is stronger?

Which AA are required for purine synthesis?

Back 4

Purines are double ringed bases comprised of Guanine and Adenine. Their synthesis requires Glycine, Aspartate, and Glutamine. GA's are PURe, they wear glasses, and often GAG.

Pyrimidines are only single ring bases comprised of Cytosine, Uracil, and Thymine. CUT the PIE (Py).

Front 5

Which de novo synthesis starts with sugar and phosphate to form PRPP? Which starts with a temporary base?

Back 5

Purine de novo synthesis starts with PRPP while the pyrimidine de novo synthesis starts with a temporary base (orotic acid) that we build upon. In purine synthesis the base is added last.

Front 6

What is the common pathology associated with a defect in pyrimidine synthesis? It typically presents with megaloblastic anemia that does not improve with administration of vitamin B12 or folic acid?

Back 6

Orotic Aciduria

A deficiency in either orotic acid phosphoribosyltransferase or orotidine 5'-phosphate decarboxylase enzymes--inability to convert orotic acid into UMP. Pt will also present with orange crystal in urine, failure to thrive, and no hyperammonemia.

Be careful to distinguish for urea cycle deficiency that can also cause orotic acid to build up. Ornithine transcarbamoylase deficiency causes an increase in carbamoyl phosphate which is converted to orotic acid. It present with hyperammonemia though.

Front 7

What is the role of adenosine deaminase? If defective, what are the major affects?

Back 7

Adenosine deaminase is a crucial enzyme in the purine salvage pathway. It deaminates adenosine into inosine in order to make more IMP.
Its deficiency is a common cause of SCID or bubble boy. A build-up of ATP and dATP inhibit ribonucleotide reductase (forms deoxynucleotides) and block DNA synthesis. This hurts cells that are actively replicating like our T and B lymphocytes.

Front 8

Hypoxanthine and Guanine are further degraded into what pathways of molecules?

Back 8

They are degrade into xanthine and further into uric acid. Thus when the salvage pathway is blocks, HGPRT deficiency, uric acid builds up and cause gout and other symptoms.

Front 9

A deficiency in HGPRT causes what pathology?

Back 9

Lesch-Nyhan syndrome
This is an X-linked recessive syndrome. Commonly presents with self-mutilation, retardation, gout, and choreoathetosis.
Normally, HGPRT converts hypoxanthine into IMP and guanine into GMP as part of the purine salvage pathway. This pathway is responsible for over 80% of purine synthesis.

Front 10

What are the differences between these DNA mutations: silent, frame shift, missense, and nonsense

Back 10

Silent: due to tRNA wobble/degeneracy, the 3rd nucleotide of codon changes but the same AA remains
Frame shift: change resulting in misreading of further nucleotides downstream; early termination or nonfunctional
Missense: results in a new AA however the chemical structure is conserved--hydrophobic for hydrophobic
Nonsense: results in early stop codon; Stop the Nonsense

Front 11

What is the difference between DNA pol I and DNA pol III?

Back 11

DNA pol I degrades the RNA primer and fills in the gap with DNA.

DNA pol III elongates the leading and lagging strands during DNA replication. It also has exonuclease proofreading activity.

Front 12

What is nucleotide excision repair?

Back 12

Nucleotide excision repair: A specific endonuclease release the damaged nucleotide, DNA pol and ligase fill and reseal.

Mutated in xeroderma pigmentosum: can't repair thymidine dimers from UV light damage

Front 13

What is base excision repair?

Back 13

Base excision repair: specific glycosylases remove damaged base, AP endonuclease cuts DNA, empty sugar is removed, and gap is filled and sealed.

Front 14

What is mismatch repair?

Back 14

Mismatch repair: Unmethylated, newly synthesized strand is recognized, mismatched nucleotide is removed, the gap is then filled and sealed.

Mutated in hereditary nonpolyposis colorectal cancer

Front 15

What are the basic characteristics of the three RNAs? Which eukaryotic RNA polymerase transcribes them?

Back 15

tRNA: tiny; RNA pol III
mRNA: massive; RNA pol II
rRNA: rampant; RNA pol I

The RNA pols are named in the order that the RNAs are used. They also do no proofread as DNA pols do.

Front 16

What are the nonsense codons?

Back 16

UGA: U Go Away
UAA: U Are Away
UAG: U Are Gone

Front 17

What are the start codons for both eukaryotic and prokaryotic cells? What AA does it code for.

Back 17

The only start codon is AUG. In eukaryotes it codes for methionine while in prokaryotes it is a formyl-methionine.

Front 18

What are the three regions that regulate gene expression?

Back 18

The promoter, enhancer, and silencer.

Front 19

Tell me about the promoter region?

Back 19

Site where RNA pol and other TFs bind. Typically AT-rich and has a TATA box. It is not the actual start site, that is the AUG codon.

Front 20

Tell me about enhancer and silencer regions?

Back 20

They both can be located close to, far from, or even within the gene whose expression it regulates.

Enhancers are sites for TFs to bind which increase expression. Silencers are for repressors and they decrease expression.

Front 21

What are that main processing components of hnRNA (pre-mRNA)

Back 21

The main components include 5' capping, polyadenylation on 3' end, and splicing out of introns. Once complete, it is termed mRNA.

Front 22

What is the main processes in pre-mRNA splicing?

Back 22

The snRNPs and other proteins form the spliceosome, a lariat is formed, and the two adjacent exons are joined.

Patients with lupus makes abs to the snRNPs.

Specific A in the middle of the intron is targeted by a GU at the front of the intron to form loop.

Front 23

How do glucose and lactose influence the lac operon?

Back 23

If lactose is present in sufficient quantities, it needs to be degraded. Lactose binds the repressor of the lac operon to allow production of lac genes to degrade lactose.

If glucose is present, then there is no need for the lac operon products. Glucose blocks cAMP production and consequently the CAP activator to repress lac operon gene expression.

Front 24

What are introns and exons? What does alternative splicing allow?

Back 24

Introns are intervening noncoding segments of DNA.

Exons contain the actually genetic information and are eventually expressed. Exons are expressed.

Alternative splicing allows for different combinations of exons based on the regulatory proteins present. This means that the same gene can make different proteins in different tissues of the body by combining and/or skipping exons.

Front 25

Explain the structure of tRNA

Back 25

tRNA is the smallest of the RNA structures. Its secondary structure is a cloverleaf form. At the 3' end it has a CCA sequence that covalently binds AAs.

CCA--Can Carry Amino acids

Front 26

What is the process of charging tRNAs?

Back 26

tRNAs are charged by the aminoacyl-tRNA synthetase enzyme. Each enzyme matches only one AA, however each can interact with multiple tRNAs due to the degeneracy of the codons. The enzyme is responsible for the accuracy of the AA selection.

The mechanism requires burning ATP into AMP; so 2 phosphates are used to form the covalent bond.

Front 27

What is the tRNA wobble theory?

Back 27

The theory states that only the first two AAs of a codon actually matter and that the third can vary due to the degeneracy of the codon in our DNA.

Front 28

Which ribosomal subunits are used in prokaryotes and which are used in eukaryotes?

Back 28

PrOkaryotes have the Odd numbered subunits: 30s, 50s, and 70s all together.
Eukaryotes have the Even numbered subunits: 40s, 60s, and 80s all together.

Front 29

What role do ATP and GTP play in protein synthesis?

Back 29

ATP Activates tRNAs; it is converted to AMP when tRNA is charged with an AA.

GTP allows the tRNA to Grip the ribosomes. Its hydrolysis triggers initiation of protein synthesis.

Front 30

What component of the ribosome catalyzes the peptide bond transfer for the growing polypeptide chain?

Back 30

rRNA or ribozymes catalyzes this bond formation and allow the polypeptide to grow.

Front 31

Do AAs recognize the stop codon to terminate protein synthesis?

Back 31

No, it is recognized by a releasing factor. The completed protein is then released from the ribosome and the RF triggers dissociation of the ribosome.