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63 Cards in this Set
- Front
- Back
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G1 Phase
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Young, metabolically active, 46 Chromosomes (not dense yet)= 46 strands of DNA
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S Phase
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every double helix is copied (number of chromosomes does not change) 1 Chromosome=> 2 sister chromatids of a centromere
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G2 Phase
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no change in chromosomes...
metabolism and growth prepare for M Phase |
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M Phase
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division into 2 new daughter cells
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Karyotype
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picture of 23 chromosomes
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Homologous
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Similar information @ same loci= 1 mat. and 1 pat.
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Diploid
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2n, genes in pairs
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TDF gene
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testis determining factor;
females develop in the absence of TDF |
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Mitosis
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diploid-->1 division--> 2 diploid cells (genetically identical to each other and parent cell)
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Meosis
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diploid--> 2 divisions--> 4 haploid cells (in gametes, chromosome # is halved)
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Mitosis- Prophase
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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. |
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Mitosis- Metaphase
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Line up at center of cell
Once everyone is captured by a spindle fiber= Anaphase |
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Mitosis- Anaphase
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Depolymerization of the spindle fibers= pulling sister chromatids= CHROMOSOME(not a sister chromatid)
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Mitosis- Telephase
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Chromosome begin to decondense
Forms new nuclear mb Cytokinesis= New cells(diploid) just not duplicated yet |
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Meosis- Prophase I
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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 |
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Meiosis- Metaphase I
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spindle fibers are forming kinetochore
2 lines of 23 pairs across from each other |
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Meosis- Anaphase I
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depolymerization of spindle fibers
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Meosis- Telephase I
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cytokinesis
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Meosis II
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same as Mitosis
4 independant haploid cells |
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Spermatogenesis
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spermstogonium-> matures into primary spermatocyte-> meiosis I
2 spermatocyte--> Meoisis II--> haploid spermatotids |
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spermatogonium
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arise from testicular stem cells
each stem cell divides into 1 spermatogonium and 1 stem cell (70 day cycle) |
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Oogenesis
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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
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sperm entry into ovum triggers what?
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Meoisis II
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Alleles
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forms of a gene
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Monohybrod cross genotype
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1:2:1
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Monohybrid cross Phenotype
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3:1
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Test Cross
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testing for the allele of an unknown
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Carriers
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possess on recessive copy but does not express the trait
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Modes of Inheritance
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X linked dom
X linked rec Y linked Auto dom Auto rec |
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Achondroplasia
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Autosomal dominant
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If parents look the same and are capable of having babies that look different they are...
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HYBRID
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Red/ Green color blindness
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X linked recessive
affects mostly men |
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Duchene Muscular Dystrophy
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X linked recessive
disproportionately affects women |
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Ricketts
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X linked dominant
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Polydactyly
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Autosomal Dominant
Limited Penetrance 90% |
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Variable Expressivity
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the degree to which the affected people show it.
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Limited penetrance
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% of people who inherit the gene who show the trait
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Bending Theory
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blend parents
i.e. black + white= grey |
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Snap Dragons
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incomplete dominance
Red Pink and white |
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Epistasis
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the expression of one gene can affect the expression of another
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Albinism
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Epistasis
lack on melanin producing enzyme |
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X chromosome
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vital for life
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Bar body
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in female; one X is being expressed and used , the other X chromosome is being compacted and for the most part inactivated= bar body
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Mosaics
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women- not every cell is reading different X chromosomes
Calico cats= patches of orange and red |
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CoDominance
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if you inherit 2 different alleles of a gene, you express both
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ABO Blood type
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CoDominance and multiple alleles
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When every generation is affected...
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Dominant
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Prader Willi Syndrome
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deletion of a piece of chromosome 15 on the paternal chrom.
-short -mild--> moderate MR -poor msl tone -hypogonadia -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 |
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Imprinting
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inaccessible on that particular chromosome (there something blocking that gene)
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Angelman Syndrome
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deletion of a piece of chromosome 15 on the maternal chromosome
-severe MR -seizures -perpetual smile -uncoordinated gate (ataxia) -the complement on the paternal chromosome is imprinted |
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Sex Influenced
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Sometimes it may affect males (dominant) differently that females (recessive)
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Male Pattern Baldness
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Autosomal Allele
behaves as dominant in males and recessive in females |
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Mitochondral DNA (mtDNA)
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mutates very rapidly
no proofreading fx--> mutations are not edited out This is a problem in tissues that have heavy need for ATP |
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Mitochondral Inheritance
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all from mother
we do not receive paternal mtDNA |
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Mitochonral Myopathies
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a series of disorders the affect skeletal msls
severe fatigue |
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Levels of Variable Expressivity
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How many bad mt you have
which tissue has them how long it takes to accumulate them |
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Leiber Hereitary Optic Neuropathy (LHON)
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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**** |
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Gene expression
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protein synthesis
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Mutations
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rare chance events that alter the sequence of NA
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3 Types of Mutations
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1. Substitution
2. Insertion 3. Deletion |
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Substitution
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base is removed and subed with another base
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Insertion
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extra base is added to your sequence (FRAME SHIFT MUT)
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Deletion
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one base is removed (FRAME SHIFT MUT)
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