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107 Cards in this Set

  • Front
  • Back
meiosis
special cell division
-used for sexual reproduction
-1/2 chromosome number
-haploid (n) gametes(sperm/eggs)
homologous chromosomes
chromosomes of same type, length, and centromeres in same place, same traits are located at exact same positions, similar staining patterns
prophase I
-each chromosome is duplicated-2 ID sister chromatids-->2 homologous pairs
1. physically match themselves (homolgous pairs) up to form tetrad
2. recombination
metaphase I
homologous pairs line up in center
anaphase I
homolgous chromosomes that seperate
telophase I
2 recombined sister chromatids on each side of cell
cytokinesis I
two daughter cells
interkinesis
similar to mitotic interphase
usually shorter
no replication of DNA (no s phase)
meiosis creates genetic variation in 3 key ways
-crossing over btwn homologues
independent assortment of homologoues
fertilization
crossing over-recombination
prophase 1
nucleoprotein lattice (synapotonemal complex) appears
-keeps homologous chromosomes (tetrad) attached
-perfectly balance exchange of DNA
-holds DNA molecules together/aligned
exchange of genetic material btwn nonsister chromatids (homolohous chromosomes)
homologues separate and go to different daughter cells
chiasmata
point where crossing over occurs
independent assortment
when homologues align at metaphase plate (metaphase I)
-align and separate in a random order
-maternal vs. paternal homologous separate randomly
causes random mixing (2^n combinations)
sexual reproduction
how genetic combinations allows species to survive in changing environment/condition
-why we need genetic variation
asexual reproduction
genetically identical clones
-love stable environments
phase of meiosis II
similar to mitosis
-almost the same as mitosis of 2 haploid but no DNA replication in interkinesis
Prophase II
-chromosomes condense
-spindle fibers start to form from centrosomes
Metaphase II
-2 sister chromatids align along metaphase plate
anaphase II
2 sister chromatids seperate
telophase Ii
reformation of nuclear envelope
cytokineses II
cell division
-at end 4 haploid cells geneticaly unique
meiosis v mitosis
2 nuclear divisions v. 1 nuclear division
halves chromosome number v same chromosome number as parent cell
4 daughter cells v 2 daughter cells
daughter cells genetically different from parent and to each other v daughter cells genetically identical to parent and to eachother
used only for sexual reproduction v used for asexual reproduction and growth
spermatogensis
production of sperm
-all 4 cells become sperm in meiosis (in moles)
oogensis
production of eggs
-only 1 of 4 nuclei get cytoplasm
-becomes the egg/ovum
-others wither away as polar bodies
zygote
zygote
undergoes mitosis-->multicellular embryo
each somatic cell=same number of chromosomes/genetic makeup as zygote
primary spermatocyte
(2n)
-in meiosis one will produce 2 secondary spermatocytes
-in meiosis Ii will produce spermatids that are haploid
primary oocyte
(diploid)
-meiosis I-nuclear division but uneven cytoplasm division
-->first polar body withers away and dies
-only one egg cell
-meiosis I is completed after entry of sperm
-->second polar body dies
-->one diploid zygote
clomid
reads with all body tissues that have estrogen receptors
-fads the body into believing that estrogen level low
-body makes more hormones-->ovulation
karyotyping
-numbered according to size (long-->short)
detect major defect/add on
-detect sex of species
monosomy
(2n-1)
one of a chromosome pair is missing
-processing occurs with problem in meiosis=non-disjunction
trisomy
(2n+1)
3 copies of same chromsome
non-disjunction
nondisjunction case 1
don't separate chromosomes the way suppose to be
-all 4 homologous chromosomes go in same direction during anaphase 1
-gametes: 2 cells: n+1, 2 cells: n-1
nondisjunction case 2
normal meiosis 1
in meiosis II problem with sister chromatids seperating
gametes: n+1, n-1, n, n
phenotype
appearance of indicidual based on genetics
turner syndrome(XO)
monosomic for X chromosome
-femal, normal intellegence/function
klinefelter syndrome (XXY)
-male
-->underdeveloped testes, enlarged breast growth
-->normal intelligence
-->presence of y always male
deletion
missing a section(several genes0 of DNA
duplication
region of DNA repeated on same chromosome
translocation
part of a chromosome moves to a non-homologous chromsome
inversion
2 breaks in a chromosome where a section of DNA becomes inverted and then reattached
deletion syndromes
williams syndrome-part of chromosome 7 deleted
philadelphia chromosome
if translocated can activate cancer-causing gene
ex: move from #9 (under control) to #22 (cranked out)
garden pea
-grown easily in large numbers
-reproduction can be manipulated
-both male/female can self and cross-polinate
mendel's traits
flow color
flower position
seed color
seed shape
pod shape
pod colour
stem length
true-breeding
result will be all dominant trait
monohybrid cross
looked at one trait at a time
law of ssegregation
during formation of sperm and egg cells (meiosis) alleles separate (each gamete only inherits one allele)
genotype
2 alleles an individual has for a specific trait
punnet square
table listing all possible geneotypes resulting from a cross
test cross
determine genotype of individual with dominant phenotype
-crossing a plant with unknown fenotype (Tt, TT) with a plant that is (tt) homozygous recessive
two-trait inheritance
dihybrid cross uses true-breeding plants differing in two traits
law of independent assortment
pair of factors for on trait segregate independently of those for other traits
all possible combinations can occur in gametes
gene linkage
several genes on the same chromosome
-tend to be inherited together
-if all genes on same chromosome than independent assortment doesn't apply
recobinants
sister chromatids that have recombined in a new way that is not predicted by punnet squares
-farther apart the genes, the more likely recombination will occur
tay-sachs disease
progressive, neurological condition
-fatal by age 5
-both parents must be carriers
-autosomal recessive
cycstic fibrosis
-affects respiratory and pancreas
-a lot of infections because of mucous buildup
autosomal recessive
sickle cell anemica
-provides resistance against malria
-heterozygous genotype will have some sickle cell RBCs
autosomal recessive disorders
-most affected children have unaffected parents
-heterozygotes (Aa)have unaffected parents
-heterozygotes have an unaffectd pheonotype
-two affected parents will always have affected children
-affected individuals with homozygous unaffected mates will have unaffect children
-close relatives that reproduce are more likely to have affected children
-both males and females are affected with equal frequencies
huntington's disease
-neurological disorder
-progressive degeneration of brain cells
-stuttering alleles (anticipation)
-->increase in each generation
hypercholesterol
heterozygous-mild disease
homozygous dominant-abilty to make LDL receptors
homozygous recessive inability to make LDL receptors
Autosomal dominant disorders
-affected children will usually have affected parent
-heterozygotes are affected
-2 affected parents can produce an unaffected child
-2 unaffected prents will not have affected children
-both males and females are affected with equl frequency
y-linked
-genes on y chromosome
-only inherited from dad
-only gives to sons
mitochondrial disorders
-mostly inherited from mom
-sperm to streamline to have mitochondria
x-linked alleles
-genes carried on the x chromosome
-different pattern of inheritance
-depends on whether female/male
-males only recieve one X so either have disease or dont
color vision
-blue sensitive gene is autosomal
-red and green sensitive genes on x chromosome
x linked recessive disorders
-more males than females affected
-affected son can have parents who have normal phenotype
-for female to have characteristic, father must also have it. mother must have it or be carrier.
-often skips generation from grandfather to grandson
-if women has characteristic than all sons will have it
hemophilia
bleeder's disease
-bleed to death from simple bruises
-mostly males are affected
incomplete dominance
-heterozygote has phenotype intermediate btwn that of either homozygote (matches blending theory)
-phenotype tells wht the genotype is (no need for test crosses0
-ex: red and white flowers-->pink
blood type
-four different phenotypes
-A, B, AB, O
-2 alleles dominant, one is recessive
polygenic inheritance
-phenotype controlled by two or more genes
-each dominant allele has an effect on the phenotype
-effects are additive
-continous variation of phenotypes
pleiotropy
-one gene interferes with the expression of another gene
-albino and eye color genes
enivornmental effects
ex: rabbit fur is temperature dependent
-type II diabetes
lethal alleles
some combinations of alleles never make it to phenotype
stuttering alleles
-more severe symptoms each succeeding generation
-earlier onset
-repeat elements duplicate in each generation
gender-related effects
genes that have a different effect depending on which parent inherited from
-some rare inherited diseases
mosaicism
genes inherited by both male and female but expressed differently in the phenotypes
fredrick griffith experiment
-virulence passed from dead to living strain
-transformation
transformation
Avery
-DNA from dead cell was being incorprated into DNA of living cell
viruses
protein coat and nucleic acid core
bacteriophages
bacterial viruses
hershey and chase
reproduction of viruses
-DNA not the protein enters the host
-DNA of the phage is genetic info
chargaff's law
the amount of A in a DNA molecule must euqal the number of t
A=T
G=C
Meselson-Stahl experiment
semi-conservative model of DNA replication
-found by heavy and light nitrogen and how hybrid entertwines not with eachother but with one of the original parent strands
semi-conservative
as DNA parent strands separate each strand serves as template
DNA replication
-one dughter strand synthesized continously
-other daughter strand synthesized in pieces
-->antiparallel strand
helicase
seperates the two strands
-enzymes need to access the bases to read them and know what pairing ares needed for new strand
SS binding proteins
-single stranded
-keep two strands from sealing up aftrer helicase by covalent bonds
primase
RNA polymerase
-helps kickstart
-everytime helicase opens strands primase will put RNA (temporary fix) to start DNA synthesis
semi-discontinous
-one strand continously replicated (leading)
-other has helicase and RNA breaks (lagging)
DNA polymerase
replaces RNA primers
DNA ligase
seals up niches-continues DNA molecule
-Ozawaki fragments go away
prokaryotiuc v eukaryotic
pro-starts at one loction
-eu-many origins of replications (linear)
Nucleoside Analogs
block DNA replication
-high toxicity
-->any rapid growing cell affected
-used against viruses
-->virus and cancer cells replicated fast
-not selective
function of genes
-genes encode proteins (enzymes)
-segment of DNA that encodes a sequence of amino acids
genetic mutation
changes of the nucleotides (A,G,C,T)
might change primary structure/shape?
might change function of protein?
RNA
polymer of U,A,C,G ribonucleotides
-not as stable as DNA
messenger RNA (mRNA)
intermediate btwn DNA and protein
transfer RNA (tRNA)
molecular/nucleic acid language-->another language (amino acid)
ribosomal RNA (rRNA)
along with protein packaged up to make ribosomes structurally and functionally
Transcription
-gene unzips
-RNA nucleotides bind to exposed DNA bases
-complementery to DNA
-RNA polymerase connects nucleotides
transcription initiation
special sequences in DNA that tell RN polymerase to bind or not bind
-RNA polymerase very attracted to promoter DNA
transcription elongation
RNA polymerase will read section
transcription termination
growing RNA ends at terminator DNA
-completed RNA
translation
-mRNA travels to cytoplasm throuhg nuclear pores
-associate and bind to a ribosome
-ribosome reads mRNA in 3 nucleotide words (codons)
-ribosome catalyze peptide bonds
-amino acids will be added sequentially
translation initiation
-start at AUG (methionin-1st amino acid of every protein)
-3 binding sites: E,P,A
genetic alphabet
U, A, G, C
Translation Elongation
-tRNA anticodon binds to mRNA codon (A site)
-peptide bond formed
-tRNA (w/protein attached) moves to P site
-empty tRNA exits from E site
-cycle continues
Translation termination
-ribosome reads the STOP codon t the end of the mRNA
-release factor
-mRNA can be reread or broken down