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63 Cards in this Set

  • Front
  • Back
G1 Phase
Young, metabolically active, 46 Chromosomes (not dense yet)= 46 strands of DNA
S Phase
every double helix is copied (number of chromosomes does not change) 1 Chromosome=> 2 sister chromatids of a centromere
G2 Phase
no change in chromosomes...
metabolism and growth prepare for M Phase
M Phase
division into 2 new daughter cells
picture of 23 chromosomes
Similar information @ same loci= 1 mat. and 1 pat.
2n, genes in pairs
TDF gene
testis determining factor;
females develop in the absence of TDF
diploid-->1 division--> 2 diploid cells (genetically identical to each other and parent cell)
diploid--> 2 divisions--> 4 haploid cells (in gametes, chromosome # is halved)
Mitosis- Prophase
1. Coiling on DNA around Histones to make diense chromosomes--> 2 dense sister chromatids with kinetochores hanging off of it
2. Nuc. Mb comes apart
3. Polymerization into tubules= organization of microtubules into 2 fibers at either end of cell= spindle fibers==> one captures each sister.
Mitosis- Metaphase
Line up at center of cell
Once everyone is captured by a spindle fiber= Anaphase
Mitosis- Anaphase
Depolymerization of the spindle fibers= pulling sister chromatids= CHROMOSOME(not a sister chromatid)
Mitosis- Telephase
Chromosome begin to decondense
Forms new nuclear mb
Cytokinesis= New cells(diploid) just not duplicated yet
Meosis- Prophase I
1. condense DNA into managable packages
2. homologous pairs physically come together to form 23 couples
3. random crossing (tetrads) over occurs b/w mat and pat
4. nuc mb comes apart
5. polymerization of microtubules
Meiosis- Metaphase I
spindle fibers are forming kinetochore
2 lines of 23 pairs across from each other
Meosis- Anaphase I
depolymerization of spindle fibers
Meosis- Telephase I
Meosis II
same as Mitosis
4 independant haploid cells
spermstogonium-> matures into primary spermatocyte-> meiosis I
2 spermatocyte--> Meoisis II--> haploid spermatotids
arise from testicular stem cells
each stem cell divides into 1 spermatogonium and 1 stem cell (70 day cycle)
Oogonium--> primary oocyte--> meiosis I (cytoplasmic division not equal= nucleus is on one side)--> 1- secondary oocyte and 1 polar body(little cytolasm= cell will disintegrate)--> meosis II --> 1 ovum and 3 polar bodies
sperm entry into ovum triggers what?
Meoisis II
forms of a gene
Monohybrod cross genotype
Monohybrid cross Phenotype
Test Cross
testing for the allele of an unknown
possess on recessive copy but does not express the trait
Modes of Inheritance
X linked dom
X linked rec
Y linked
Auto dom
Auto rec
Autosomal dominant
If parents look the same and are capable of having babies that look different they are...
Red/ Green color blindness
X linked recessive
affects mostly men
Duchene Muscular Dystrophy
X linked recessive
disproportionately affects women
X linked dominant
Autosomal Dominant
Limited Penetrance 90%
Variable Expressivity
the degree to which the affected people show it.
Limited penetrance
% of people who inherit the gene who show the trait
Bending Theory
blend parents
i.e. black + white= grey
Snap Dragons
incomplete dominance
Red Pink and white
the expression of one gene can affect the expression of another
lack on melanin producing enzyme
X chromosome
vital for life
Bar body
in female; one X is being expressed and used , the other X chromosome is being compacted and for the most part inactivated= bar body
women- not every cell is reading different X chromosomes
Calico cats= patches of orange and red
if you inherit 2 different alleles of a gene, you express both
ABO Blood type
CoDominance and multiple alleles
When every generation is affected...
Prader Willi Syndrome
deletion of a piece of chromosome 15 on the paternal chrom.
-mild--> moderate MR
-poor msl tone
-obese (eat constantly= hyperphagia, choking is a big problem)
-maternal chromosome will not compensate--> maternal chrom is inaccessible- you can't express the healthy genes
inaccessible on that particular chromosome (there something blocking that gene)
Angelman Syndrome
deletion of a piece of chromosome 15 on the maternal chromosome
-severe MR
-perpetual smile
-uncoordinated gate (ataxia)
-the complement on the paternal chromosome is imprinted
Sex Influenced
Sometimes it may affect males (dominant) differently that females (recessive)
Male Pattern Baldness
Autosomal Allele
behaves as dominant in males and recessive in females
Mitochondral DNA (mtDNA)
mutates very rapidly
no proofreading fx--> mutations are not edited out
This is a problem in tissues that have heavy need for ATP
Mitochondral Inheritance
all from mother
we do not receive paternal mtDNA
Mitochonral Myopathies
a series of disorders the affect skeletal msls
severe fatigue
Levels of Variable Expressivity
How many bad mt you have
which tissue has them
how long it takes to accumulate them
Leiber Hereitary Optic Neuropathy (LHON)
mt disorder
-progressive degeneration of optic nerve
-kicks in during 20s, some vision loss
-loss of central vision--> loss of color vision--> optic nerve degnerates--> total blindness
-optic nerve has very high need for ATP
****cytoplasmic donation is the only way to avoid this****
Gene expression
protein synthesis
rare chance events that alter the sequence of NA
3 Types of Mutations
1. Substitution
2. Insertion
3. Deletion
base is removed and subed with another base
extra base is added to your sequence (FRAME SHIFT MUT)
one base is removed (FRAME SHIFT MUT)