KA BIOMOLECULES Flashcards

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1
Q

noncoding rna

A

functional RNA that skips the step of translation and carries out functions in its own
• ex: ribosomal RNA, transfer RNA (both used for translation of mRNA to proteins)

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2
Q

epigenetics

A

study of heritable changes in DNA activity that are not caused by changes in DNA sequence
• unlike traditional genetics, where DNA sequences determines phenotype, epigenetics describes how phenotypes can be modified without actual changes in nucleotide sequence
• Main mechanisms of epigenetics: DNA methylation and histone modification
• Epigenetics also explains how DNA in muscle cells is identical to DNA in skin cells, but the cells are very different because of different expressions. Epigenetics explains how different parts of the sequence are expressed.

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3
Q

are beta parallel or antiparallel bonds stronger?

A

anti parallel bc the h bonds are stronger and linear whereas the former r bent bonds

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4
Q

isoelectric point (pi)

A

the point along the pH scale where the amino acid has a net 0 charge.
• This also means the AA is least soluble, and does not migrate in an electric field.

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5
Q

pka

A

a measure of the tendency of a group to give up a proton

buffer zone

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6
Q

what types of bonds make up the primary structure

A

peptide and covalent

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7
Q

what rxn forms peptide bonds and what cleaves them

A

nucleophilic addition/eleimaation (dehydration synthesis)

latter is hydrolysis

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8
Q

what aa are good for strong alpha helix

A

ala and leuc since they are small enough but wont cause any kinks

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9
Q

operator vs promoter

A
  • operator - sequence of DNA to which a transcription factor protein binds
  • promotor - sequence of DNA to which RNA polymerase binds
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10
Q

enhancer

A
  • enhancers are usually cis-acting (acting on the same chromosome), but they don’t need to be particularly close to the gene they’re acting on.
  • enhancers don’t act on promotor region themselves, but are bound by activator proteins which can interact with mediator multiple protein complex. (Complex recruits RNA pol. and GTFs, leading to transcription of the gene.)
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11
Q

inducer

A

(molecule that initiates gene expression, like lactose with the lac operon) is present, it can interact with repressor in a way that causes it to detach from the operator so RNA pol. is free to further transcribe gene.

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12
Q

name the 2 types of rna editing (keep in mind that is rare)

A
  • “Adenosine Deaminase Acting on RNA,” aka ADAR, is one type of RNA editing which converts specific adenosine residues to inosine in an mRNA molecule by hydrolytic deamination.
  • CDAR - involves deamination of cytosine to uridine by cytosine deaminase.
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13
Q

• MicroRNA (miRNA)

A

functions in transcriptional and post-transcriptional regulation of gene expression by base pairing with complementary sequences within mRNA molecules.
• This usually results in gene silencing. The mRNAs to which miRNAs bind are prevented from translation or sent through a pathway for degradation.

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14
Q

polyadenylate polymerase,

A

• Poly-adenylation is catalyzed by the enzyme polyadenylate polymerase, which adds adenine molecules using ATP as substrate. The poly-A tail is built until it’s about 250 nucleotides long.

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15
Q

• Small nuclear RNA (snRNA)

A
  • avg. length is ~150 nucleotides. Primary function is in processing of pre-mRNA in the nucleus. They also aid in regulation of transcription factors or RNA polymerase II, and maintaining telomeres.
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16
Q

• What happens to make proto-oncogenes into oncogenes? 3 possibilities:

A

deletion or point mutation
Gene amplification / increase in mRNA stability
Chromosomal Rearrangement

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17
Q

pRb tumor suppressor gene

A
  • prevents cell from replicating when its DNA is damaged by preventing progression of the cell cycle from G1 phase to S (synthesis) phase. It binds and inhibits the transcription factors that normally push cell into S phase.
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18
Q

cyclin cdk complex

A

Cyclin-CDK complex is responsible for pushing cell from G1 to S phase.

19
Q

why is p53 considered a dominant negative

A

• exception to the two-hit hypothesis occurs with certain mutations of p53, which can then result in a dominant negative, meaning a mutated p53 protein prevents the protein product of the normal allele from functioning.

20
Q

spontaneous mutation

A

: person suddenly gets a mutation in their DNA without their parents having it.
• can come from DNA replication errors, environmental factors, or be completely random

21
Q

name the 2 type of missense mutations

A
  • Missense mutation: any genetic mutation that changes an amino acid from one to another.
  • Conservative mutation: new AA is the same type as the original (ex: Glu —> Asp, both are acidic)
  • Non-conservative mutation: new AA is different type than the original (ex: Ser (polar)—> Phe (non-polar, aromatic))
22
Q

what are frameshift mutat

A

one DNA base is added to the gene sequence. This leads to an additional base in the mRNA sequence, which changes the reading frame (codons) of the mRNA during translation. All codons (and corresponding AA) that come after the extra base will be slightly different.
• Frame-shift mutations have a more significant effect on final protein than point mutations

23
Q

frameshift mutat are caused by

A
  • Insertion: extra DNA base finds its way into our sequence, leads to an extra mRNA base, which shifts codon reading frame and throws off following amino acids
  • Base deletion: one DNA base is dropped from original sequence. Also results in a shift of mRNA reading frame.
24
Q

large scale mutations are:

keep in mind that theyre not point or frameshift

A

exist at chromosomal level & affect many genes instead of a few base pairs

  • These large scale mutations don’t always affect individual nucleotides, but many of these types of mutations affect how a gene’s expression is regulated, in addition to changing what the genes actually code for.
  • Remember that the position of the gene on the chromosome partly determines how it’s regulated (b/c of histone modification, promotor sequences, etc.)

ex: translocation and chromosomal inversion

25
Q

chromosomal inversion

A

two genes on same chromosome switch places

26
Q

intercalators

A

type of exogenous mutagen

ex: Ethidium Bromide (EtBr) - it jumps into a DNA helix and sticks itself between the two strands. When these intercalators “intercalate” into DNA, they can deform structure of DNA and cause serious problems.

27
Q

base analog

A

type of exogenous mutagen

: pretend to be certain bases but acts differently.
• ex: 5-Bromouracil (5-BU) looks like uracil but once it’s incorporated into DNA it can shift into two different forms (via a tautomerization reaction). In its keto form, it pairs best with adenine. In enol form, it pairs best with guanine.

28
Q

dna library components

A

• Step 1- generate DNA from mRNA:
cDNA is single stranded, so we need to add DNA polymerase to make it double stranded.

  • Step 2- sequence the double stranded DNA
  • Amplification: inject DNA into a cloning vector (such as a plasmid or a virus), which can then be added to bacteria and the bacteria will produce (clone) lots of the DNA segment.
  • Once we have lots of DNA, we can sequence it (through PCR, fluorescent labeling, and gel electrophoresis
29
Q

what is dna hybridization

A

• DNA-Hybridization is the process of combining two complementary single-stranded DNA molecules and allowing them to form a single double stranded molecule through base pairing

30
Q

micro array aka biochip is a what?

A

collection of microscopic mRNA spots attached to a solid surface. They’re attached because the chip has a bunch of really tiny wells on it, and in the wells are complementary strands (complementary to a gene’s mRNA).
• When we break a cell apart to get a the mRNA for the assay, we label it with markers. Then we put the labeled mRNA on the chip & it binds (hybridizes) to the wells with complementary nucleotides.
• Say we have a cancer cell, whose mRNA we label blue, and a normal cell, whose mRNA we label yellow. Once we put together a microarray, a computer can analyze it to tell us which genes of the cancer cell are upregulated or downregulated, based on how much of the yellow or blue marker is present for a particular gene well. If there’s no change in a cancer’s gene from a normal one, you’ll see something in the middle, like a green dot for our example.

31
Q

dna helicase vs taq polyerase

A

helicase will break the double stranded dna

taq polymerase is special bacteria enzyme that is used bc it is resistant to high heat when breaking the double strand dna for pcr methods. it makes copies of the double dna and can add bases (like its name polymerase says) but just needs a primer to do any of this stuff

32
Q

pcr method

A

exponentially

2^n (n= number of rounds of particular dna sequence)

steps:

  1. mrna needs rev transcript to turn into complement dna through heating..
  2. then amplify it with taq polymerase

• PCR can be useful in detecting if a target sequence was in a given sample because it uses specially constructed primers to amplify the specific DNA sequence. If the PCR reaction produces more nucleic acid, then the target sequence was in the sample

33
Q

dna ladder

A

The DNA ladder is a predetermined set of DNA fragments; they have known sizes. So when we run the gel, we can compare how far our DNA fragments migrated with the migration distance of the known fragment sizes, and thus estimate the approximate size of our fragments.

34
Q

why make the gel for electrophoresis for dna basic?

A

to dentaure the neg charge on the dna

35
Q

how do u use sanger sequencing to fluorscent dna labels

A

. With Sanger sequencing, you also want to add a dideoxynucleotides (ddNTP, which only has a H on C-3 instead of an OH). This will prevent elongation (because phosphate group can’t attach to the H) and your DNA sample of interest will be fragmented into different lengths

36
Q

x linked recessive for men and women

A

• If there’s a m (1/700) chance of an X-linked mutation, men have m chance of getting the disease, while woman have m2 chance (1/700 * 1/700 = 1/490000 chance)

37
Q

penetrance vs expressitivity

A

Penetrance is the probability that someone with a genotype for a disease will actually express the phenotype for the disease. So for example someone may be heterozygote for an autosomal dominant disease, but they won’t actually experience any disease symptoms.
Examples of not 100% penetrance are mutations in the BRCA1 gene that lead to familial breast cancer. I think it’s like around 65-80% penetrance which basically means that there’s a chance that even if you have the alleles for breast cancer, you may not get breast cancer. Another example is retinoblastoma which has a penetrance of about 90%.
Variable expressivity on the other hand is basically what severity of the disease you have. While penetrance is do you have the disease or not, variable expressivity is what “level” of the disease do you have.
Marfan syndrome and neurofibromatosis both have 100% penetrance. This means that if you have the disease allele, you WILL express the disease for sure. But since they also have variable expressivity, you may have a more or less severe form. Individuals have the same phenotype, but the severity of the disease is different.

38
Q

bottleneck effect

A

a situation where a population becomes very small due to an environmental stress and loses much of its genetic diversity

39
Q

e types of post zygotic isolation

A
  • (1) Zygote mortality - even if the gametes of two organisms come together to form a successful zygote, that zygote cannot develop into offspring
  • (2) Hybrid Inviability - zygote can grow into offspring, but that offspring has a high mortality rate and will not develop into an adult.
  • (3) Hybrid sterility - offspring can grow into a mature adult, but can’t produce offspring of their own
40
Q

genetic drift

A

changes in the frequency of alleles in a gene pool, simply due to chance

41
Q

gene flow

A

alterations in the composition of a gene pool due to migration of individuals between different populations

42
Q

• Remember that whenever you have a gradient in something (ph, charge, or in this case, temperature), then

A

that means potential energy is being stored up. If there’s no opposing force, that gradient wants to disappear.

43
Q

at what ends does sucrose (fructose and glucose) join?

A

• Sucrose = glucose and fructose monomers joined by a α-1,1-glycoside bond
• Unlike both both lactose and maltose (which consist of two pyranoses, or
6-membered rings), sucrose consists of one pyranose and one furanose.
• Also unlike lactose & maltose, the two monomers in sucrose are joined at both
anomeric carbons.
• With lactose and maltose (and any 1,4 glycosidic linkage), the anomeric carbon of the first monomer becomes an acetal, while that of the second carbon is still a hemiacetal. The hemiacetal can undergo another alcohol attack and be reduced further (more monomers can join via more glycosidic linkages).
• With sucrose, however, since both anomeric carbons are joined, two acetals are formed.
It’s non-reducing.