Prokaryotes reproduceasexually through binary fission, eukaryotes reproduce sexually through mitosis/meiosis
Both prokaryotes and eukaryotes can undergo aerobiccellularrespiration
Histones
Proteins that DNA wraps around for organization, too tight winding makes DNA unusable
Histones
Relate to gene regulation (when and where to make proteins) and to mitotic chromosomes (only formed when cells make new copies of themselves)
Homologous pair
Twochromosomes similar in shape and information but can have some variation (alleles)
Mitotic chromosome
Formed when cells make new copies of themselves
Centromere
Connects sisterchromatids together
Centrosome
Connects to the microtubules
Gene
Genetic information to make a protein
Allele
Variation of a gene
Phases of cell cycle where DNA is available for transcription and translation
Interphase (G1 and G2 phases)
Prophase
Telophase and Cytokinesis (Mitosis)
During S phase of interphase, DNA replication occurs which temporarily disrupts transcription
Growth factors
Regulate cell cycle progression and control processes
Checkpoints in cell cycle
G1: Check if DNA replication went well and DNA is notbroken or mutated
S: Check if DNA replication is progressing and there are enough substrates
G2: Quality control - check DNA replication and prepare for mitosis
Metaphase: Check if centromeres have centrosomes so mitoticchromosomes can be pulled to equatorial plate
If a cell fails a checkpoint, the cell cycle is halted and the cell attempts to completeDNA replication or repairdamaged DNA. If damage is irreparable, the cell may undergo apoptosis.
Ways cancer cells differ from normal cells
Multi-nucleated
Abnormal shape
Loss of specialization
No contact inhibition
Immortal (don't have defined lifespan)
Don't need growth factors
Abnormal mitosis
Causes cancer cells to look different (small, large, abnormal shape)
Spending too much time in mitosis vs interphase
Causes cancer cells to lose specialization
End replication problem
Chromosomes shorten at every S phase because primer on 5' end of lagging strand gets removed but cannot be fully filled in
Telomerase
Enzyme that increases transcription and translation, allowing cancer cells to be immortal
Proto-oncogenes
Normal genes that help cells progress through cell cycle
Oncogenes
Mutated proto-oncogenes that are more active and speed up mitosis
Oncogene mutations are dominant, tumor suppressor gene mutations are recessive
Tumor suppressor genes
Genes that regulatecell division and preventtumor formation
Functions of p53
Find damaged DNA
Transcription factor that repairsdamaged DNA
If not repairable, activate apoptosis
Tumor suppressor gene mutations are recessive because both copies need to be mutated to cause changes in cell growth and tumor formation
Apoptosis
Regulated cell death that destroys cells from the inside out
Steps in apoptosis
DNAse destroys DNA
Cell shape changes (blebbing)
Phagocytes remove cell fragments
Functions of commonly mutated cancer genes
Cell growth and survival (proto-oncogenes)
Cell fate (stem cell signaling)
Genome maintenance (DNA repair enzymes)
Diploid
Cells containing two sets of chromosomes, one from each parent
Haploid
Cells containing one set of chromosomes
Autosome
Chromosome pair not involved in sex determination, same number in males and females
Sex chromosome
Chromosome involved in sex determination (males are XY, females are XX)
Homologous chromosomes are similar in size and sequence but can have different alleles
Cell types formed during meiosis
Haploid daughter cells (meiosis I)
Haploid gametes (meiosis II)
Haploids must form to combine with other gametes and create genetic diversity
Genetic diversity is good for a population to adapt to the future and avoid inbreeding
Sources of diversity in meiosis
Synapsis/tetrad formation
Crossing over
Independent assortment
Alleles of different genes sort into gametes independently, travel on different homologous pairs