exam2 review

Chapter 10

CC chromosome structure and number

- Homologous pairs, when they physically stick together, that’s a tetrad

SEQ Binary fission

- Prokaryotes

- asexual

- cloning

SEQ HD Cell cycle

- G1

- Growth + metabolic activity

- S

- DNA replication

- G2

- Growth + metabolism activity, normal function, preparing for mitosis

- Centrosomes duplicate

- Mitosis

- Prophase, Condense, mitosis spindles, nuclear envelope disassembles

- Metaphase, chromosomes align at metaphase plate

- Anaphase, sister chromatids separate, pulled by kinetochore proteins

- telophase, nucleus envelope reforms, DNA decondense

- Cytokinesis, division of cell itself, cleavage furrow, and cell plate

- HD, ID, ploidy throughout mitosis (never changes)

Chapter 11

CC sexual and asexual

- Asexual : low e, less energy, safer, no disease, etc

- Benefit of sexual : genetic variation, if genetic is viable or new conditions, sexual

reproduction can ensure population persists

SEQ basic sexual life cycle

- Adults diploid -> meiosis -> gametes -> fuse (fertilization) -> zygote (diploid) -> grows

through mitosis

CC somatic cells vs gametes

- Basic cells vs sex cells

SEQ meiosis keeping track of ploidy

- prophase 1, tetrads form, crossing over, everything else with normal prophase

- metaphase 1, tetrads align up, independent assortment its random

- Anaphase 1, homologous pairs separate during anaphase 1

- telophase 1, regular telophase shit.

- Cytokinesis, get 2 cells that aren’t identical they are haploid

 - Ploidy changes in meiosis 1, went from diploid to 2 haploid

- 2n = 22 -> 2 cells n=11, haploid in interkinesis

- interkinesis - stage in between meiosis 1 and 2

- Meiosis 1 ——

- prophase 2, same as normal prophase

- metaphase 2, chromosomes line up on metaphase plate

- anaphase 2, sister chromatids of chromosomes separate into either daughter cell

- telophase 2, same

- cytokinesis

- now we have 4 daughter cells which are haploid, genetically unique, chromosomes that

are not duplicated

- we kept going until we didn’t have sister chromatids

Lecture 12

SEQ Mendel's work

- True breeding line, same traits that don’t trait no matter how many types they’re

breaded,

- mate P to get f1 (we get the same pheno), f1 Mate to make f2 (3:1 ratio, dominant, two

recessive)

- blending inheritance -> wrong, bc phenotype went away and came back

- phenotype - physical trait

- genotype - alleles u have

- 2 of same allele - homozygous

- 2 of different - heterozygous

CC mendel's model

- dominant - it makes the recessive

- recessive - it gets masked, if paired with dominant u wont see it.

- Monohybrid test cross - genotype, Ind with dominant, we can’t tell, so we mate them with

recessive, offspring will be 100% dominant, or will be heterozygous

Lecture 13

ID chromosomes, theory of inheritance

- genes are on chromosomes, together in groups

- Sex linkage - on sex chromosomes, X or Y

- Males are 46 XY, trait x linked, male affected, hemizgous recessive, they only have one

copy of it despite being diploid, they only got one x

- female, carrier for x linked with male who does not have trait, what is prob that offspring

has allele, female is a carrier so its a 50/50

- Whats the prob that their offspring have it? 25%

CC Homo and hetero gametic

- zw system - heterogametic different sex chromosomes, males are heterogametic,

woman are homogametic, in birds its the opposite

SEQ X inactivation

- forms Barr body that inactivates it, super dense bit of DNA that result sin x inactivation.

- It’s long term methylation

Lecture 14 DNA

SEQ DNA experiment

- Griffith - mice

- avery, mccarthy, Maclead - did the same shit

- Hersey - bacteria

- Rosalind Franklin - X-ray photos

- Watson and crick - formed the paper

SEQ DNA structure

- Double helix,

- nucleotides

- nitrogenous bases, phosphate, sugar

- backbone is made by sugar, phosphate

- phosphodiester holds the backbone

- nitrogenous bases, “rungs”

- hydrogen bonds hold the nitro bases together

- purine - two rings, big ones, A and G

- pyrimidines - 1 ring, small ones, C and T

- c=g

- a=t

- 50 purine = 50 pyrimidine, always

- complementary strands to each other

- 5’ phosphate

- 3’ hydroxyl

- 5’ -> 3’ , 3’ -> 5’ is antiparallel

SEQ DNA replication

- Template dna - starts at origin of replication

- helix - opens up the hydrogen bonds

- replication bubble - ?

Lecture 15 Gene expression

SEQ flow of genetic infromation

- DNA -> RNA -> polypeptide

- Transcription. Translation

TYPES of rna

- mRNA - messenger rna, encodes amino acids

- tRNA - carries amino acids to ribosome, anticodon

- rRNA - enzymatic properties , catalyzes, ribozyme

SEQ transcription

 - Initiation, elongation, termination

- We RNA poly, attaches to promoter

- origin of replication for dna replication, transcription starts at promoter

- when it attaches to promoter, rna poly unwinds and opens up dna

- starts copying just one strand, only one complementary strand

- uracil instead of t, get 5’ and 3’ correct

- Elongation Same as replication, dif enzyme

- termination sequence (dna sequences that forces shit to stop) makes it stop, forces rna

poly to stop

- We need to do 3 things to mRNA

- we had poly a tail to 3’ and CAp to 5”

- we remove the introns, splicing

- we put the extons together, which we use

SEQ translation

- initiation, elongation, termination

- initiation, mRNA att

CC : DNA replication, transcription, translation

Lecture 16 gene regulation

- Operon - region of rna, contains genes, and regulatory stuff for those genes

- operator, promoter, 3 genes

- operator - off switch

- repressor - turns operator off

SEQ, HD lac operon

SEQ eukaryotic gene regulation

- Chromatin, methylate, it gets condenses, it becomes heterochromatin

- it diffuses gets more loose its euchromatin

- Transcription

- Proteins : transcription factors, inhibit or promote it

- what can we do to make the rna last longer, poly A tail, longer poly A is more expression

- Alternative splicing, mix and matching exons

- Post translational regulation

- Modifying, folding,

CC : prokaryotic and eukaryotic gene regulation

- Prok do transcription, translation at the same time

- euk you regulate each step, post, before, during, etc

lecture 17

SEQ PCR

- amplify DNA, specific sequence

- components, template, primers (2) (made up of DNA primers), dntps, we need taq

polymerase

- denature (high temp)

- separating ds to ss

- annealing (low temp)

- bind to template

- Extension same as elongation (medium temp)

- Using Taq poly to build

- do cycle like 30 times and get hella shit dawg

PCR work

- if we have 1100

- we use gel electrophoresis, uses electrical charge to separate dna in terms of size

- negative charge,

- moves towards positive electrode

- small pieces move faster, larger move slower

Dideoxyriobluciec sequencing

- PCR with a twist

- primers (1) : 1 primer, ddntp (missing 3’ hydroxyl group, base is fluorescent), we do

denature, annealing, extend, but ddntp are dead ends.

- Instead of 800 nucleotides and always making complementary, at some point we

incorporate dideoxy base and we came make more (799, stop randomly, 222)

- results in DNA fragments that are different lengths

- How do we get them in order to read them, gel electrophoresis, we take population, and

run it tru gel, it’ll migrate by speed according to shape,

- PCR = get billions

- dideozyl sequencing = actually read the sequences

- read out is called a spectrogram

CC DNA replication, transcription, PCR, all of them

-