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Exam 4 Study Guide

by: Hannah Kennedy

Exam 4 Study Guide 30156

Hannah Kennedy
GPA 3.98

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This is a comprehensive and detailed study guide on Exam 4 that is testing Ch. 16, 17, 23.4, and 24
  Dr. Helen Piontkivska
Study Guide
Biology, Genetics, midterm
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This 15 page Study Guide was uploaded by Hannah Kennedy on Saturday August 13, 2016. The Study Guide belongs to 30156 at Kent State University taught by   Dr. Helen Piontkivska in Spring 2016. Since its upload, it has received 19 views. For similar materials see ELEMENTS OF GENETICS in Biological Sciences at Kent State University.


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Date Created: 08/13/16
© Hannah Kennedy, Kent State University 1 Exam 4 Study Guide—Ch. 16, 17, 23.4, 24 Ch. 16—Gene regulation in bacteria 1. Prokaryotic gene regulation a. Goal: respond to environmental stimuli in the most beneficial manner b. Key terminology: i. Gene regulation = the phenomenon in which the level of gene expression can vary under different conditions ii. Constitutive genes = unregulated genes; encode proteins that are continuously needed for the survival of the bacterium iii. Housekeeping genes = genes that aren’t regulated because you make and need them; they are not in response to the environment iv. Small effector molecules = molecules that don’t bind directly to the DNA to alter transcription; binds to an activator or repressor and causes a conformational change c. Common processes regulated at the genetic level: i. Metabolism: e.g. certain enzymes are needed for bacteria to metabolize sugars ii. Response to environmental stress: protein help bacteria survive envmtal stress and are needed only when its confronted with the stress iii. Cell division d. How to regulate genes: i. Based on the role of substrate (2 different gene types) 1. Inducible genes = genes whose expression will be up-regulated in the presence of a certain stimuli (e.g. food) a. Inducer = small effector molecule that causes transcription to increase (by doing 2 things) i. Bind to a repressor protein and prevent it from binding to the DNA ii. Bind to an activator protein and cause it to bind to the DNA b. Catabolism (i.e. breakdown of a substance where the substance being broken down is the inducer aka allolactose)—digestion 2. Repressible genes = genes that reduce the rate of transcription; usually something from bacteria but if you have access to it in the environment you no longer need to make it on your own a. Inhibitor = binds to an activator protein and prevents it from binding to the DNA to reduce the rate of transcription b. Allows bacteria to express genes only when they are needed to catabolize them where the corepressor/inhibitor is the product of enzymes activities—synthesis ii. Regulation mechanisms (2 kinds of regulation) 1. Positive regulation = regulation that induces transcription a. activator = a regulatory protein that increases the rate of transcription 2. Negative regulation = pulls repressor from promoter and turns on gene regulation a. repressor = a regulatory protein that binds to the DNA and inhibits 2. Operon a. Key terminology i. Operon = section of DNA that encodes multiple genes that has a common regulatory mechanism (“master switch”); enables bacteria to have a faster response to environment © Hannah Kennedy, Kent State University 2 ii. Polycistronic RNA = RNA encoded by the operon that contains the sequences of 2 or more genes; allows bacteria to coordinately regulate groups of genes iii. Promoter = flanks the operon and signals the beginning of transcription iv. Terminator = specifies the end of transcription 3. The lac operon—lactose metabolism in E. coli a. Key terminology i. enzyme adaptation = the observation that a particular enzyme appears within a living cell only after the cell has been exposed to the substrate for it; due to transcriptional regulation of genes b. 2 proteins necessary for the metabolism of lactose i. Beta-galactosidase—cleaves middle bond of lactose into galactose and glucose; converts a small percentage of lactose into allolactose which is used as a small effector molecule to bind to the repressor that prevents it from binding to the operator and allowing transcription of the operon to occur ii. Lactose permease—transports lactose into cells c. Lac operon components: Component What it is/does lacP - Promoter lacO - Operator - Sequence of bases that provides binding site for repressor protein lacZ, lacY, lacA - Structural genes - lacY encodes lactose permease - lacA encodes galactoside transacetylase lacI - encodes the lac repressor CAP site - DNA sequence recognized by activator protein Terminator - Terminates transcription Repressor gene - Has 2 domains 1. Capable of binding to DNA 2. Respond to allolactose d. Transcriptional regulation mechanisms: i. Inducible negative regulation (2 scenarios) (primary mechanism) 1. When lactose is absent a. lac repressor is bound to the operator site and the structural genes are not transcribed 2. When lactose is present a. binds to the repressor, a conformational change occurs in the lac repressor and it is prevented from binding to the operator site and RNA polymerase transcribes the operon ii. Catabolite repression—influenced by the presence of glucose (secondary mechanism) 1. When glucose is present a. Lac operon is repressed 2. When glucose and lactose are both present a. E. coli first uses glucose then lactose e. cycle of induction and repression 1. when lactose is available, small amount of it is taken up and converted to allolactose via beta-galactosidase. © Hannah Kennedy, Kent State University 3 2. Allolactose binds to repressor and causes it to fall off lacO 3. Lac operon proteins are synthesized which promotes the metabolism of lactose 4. Lactose is depleted and allolactose levels decrease 5. Allolactose is released from the repressor and allows it to bind to lacO 6. Proteins involved with lactose utilization are degraded f. When gene regulation is broken i. Constitutive mutants = enzymes that are produced regardless of present or absence of lactose 1. lacI gene: regulator mutations 2. lacO gene: operator mutations—unable to interact with repressor and unable to block it therefore the gene will always be on 3. lacI: gene is on all the time therefore all structural genes will be expressed in the presence AND absence of lactose 4. lacO : all structural genes are expressed constitutively + c a. lacZ alleles are also present to allow lacO to work in a single DNA molecule because g. Merozygote i. 2 important points 1. 2 lacI genes can be different alleles (one can be lacI and one can be lacI) 2. genes on F’ factor and on chromosome aren’t adjacent to each other ii. trans-effect = a form of genetic regulation that can occur even though 2 DNA segments aren’t physically adjacent: the lac repressor and activator iii. cis-effect = a DNA segment that must be adjacent to the genes that it regulates: lacO h. CAP—catabolite activating protein i. Key terminology 1. CAP = catabolite activation protein = an activator protein that mediates the effect of cAMP on the lac operon; when it binds to the promoter it creates a bend greater than 90° in DNA making the RNA polymerase easier to interact with the operator 1. cAMP = small effector molecule that is made from ATP via adenylyl cyclase; transport of glucose into the cell causes the cAMP concentration to decrease because adenylyl cyclase is inhibited 2. catabolite repression = form of transcriptional regulation that is influenced by the presence of glucose 3. catabolite = a substance that is broken down inside the cell (e.g. glucose) 4. diauxic growth = the sequential use of 2 sugars by a bacteria; nd glucose Is metabolized first then the 2 sugar ii. roles of the lac repressor and CAP in the regulation of the lac operon Sugar present cAMP levels Transcription levels What’s happening Lactose, no glucose High High cAMP binds to CAP and CAP binds to the CAP site on the lac operon and stimulates RNA polymerase to begin transcription No lactose, no High Low Binding of the lac glucose repressor due to no lactose inhibits the © Hannah Kennedy, Kent State University 4 transcription even though CAP is bound to DNA Lactose, glucose Low Low 1: The presence of lactose causes the lac repressor to be inactive 2: the presence of glucose decreases cAMP levels so the cAMP is released from the CAP preventing the CAP from binding to the CAP site No lactose, glucose Low Low Lac of CAP binding from cAMP being released from CAP and preventing if from binding to the CAP site and the repressor is bound i. regulated by 2 mechanisms—based on substrates in environment i. primary mechanism 1. Regulation that involves lactose is negative regulation therefore when repressor sits there everything is shut down ii. secondary mechanism 1. Regulation that involves glucose is positive regulation therefore when CAP is there lac operon is sitting there, then sequestered by glucose and expression levels are diminished 4. Trp operon—tryptophan biosynthesis in E. coli a. Components of the trp operon: Component What it is/does O Regulatory region trpE, trpD, trpC, trpB, trpA Structural genes that encode enzymes that take a common substrate and sequentially turn it into the AA tryptophan trpR Encodes the trp repressor trpL Mediates the attenuation regulatory mechanism b. Tryptophan levels i. When trp levels are low 1. tryptophan doesn’t bind to repressor so the trp repressor can’t bind to the operator site and RNA polymerase transcribes the operon ii. When trp levels are high 1. tryptophan acts a corepressor and binds to the trp repressor protein which causes conformation change in repressor and allows it to bind to the operator which inhibits RNA polymerase to transcribe the operon c. regulation of the trp operon i. negative regulation with a repressor © Hannah Kennedy, Kent State University 5 ii. attenuation = allows E. coli to evaluate how low we are on trp and if it needs to make more; to make trp you need to have trp in the enzymes so it can ramp up the production of its own enzymes 1. what is basically happening: regulatory mechanism in which transcription begins but is terminated before the entire mRNA is made because the mRNA from the trp operon is made as a short piece that terminates at the attenuator sequence after the trpL gene; 2. leader peptide trpL structure = evaluates how long the ribosome waits for the charged tRNA Trpto come into the A site. When it takes longer, loops will form in the tRNA; 3. stem-loops a. 3 possible loops i. 1-2 ii. 2-3 iii. 3-4: acts as intrinsic terminator so it causes RNA polymerase to pause and stop transcription b. 3 possible scenarios Scenario What’s happening Translation isn’t coupled with transcription - 1 H bonds to 2 - 3 H bonds to 4 and the terminator stem-loop forms and transcription is terminated Coupled transcription and translation under - cell can’t make sufficient amt of low trp concentrations charged tRNA trp - ribosome pauses at trp codons in trpL mRNA to wait for the charged tRNA trp - 1 is shielded - 2 H bonds with 3 - 3-4 stem loops can’t happen, terminator sequence isn’t reached, and RNA polymerase transcribes rest of operon to allow cell to make more trp Coupled transcription and translation when a - translation of trpL mRNA progresses to sufficient amt of trp is present in the cell stop codon and ribosome pauses - 2 can’t H bond with anything - 3 H bonds with 4 and terminates transcription Ch. 17—Gene Regulation in Eukaryotes 1. Prokaryotic vs. eukaryotic gene expression Prokaryotic Eukaryotic Control of transcription through specific Control of transcription through specific DNA-binding proteins DNA-binding proteins X Role played by chromatin structure Coordination achieved by operons X (aggregated transcriptional mechanisms into a few spots) X Differential splicing Attenuation X X Differential polyadenylation X Differential transport from nucleus to cytoplasm (membrane needed) © Hannah Kennedy, Kent State University 6 Differential rates of translation Differential rates of translation (membrane needed) 2. Structure of chromatin a. Key terminology i. Nucleosome = a double-stranded segment of DNA wrapped around an octamer of histone proteins; basic structural unit of chromatin ii. Histone proteins = contain a large # of charged lysine and arginine aa that can bind to DNA via electrostatic interaction and H bonds iii. Solenoid = the packing of DNA as a 30 nm fiber of chromatin; results from the helical winding of at least 5 nucleosome strands 3. Chromatin modifications a. Key terminology i. ATP-dependent chromatin remodeling = dynamic changes in the structure of chromatin that occur during the life of a cell; drives changes in the locations and composition of nucleosomes ii. Closed conformation = conformation of chromatin that makes transcription difficult or impossible iii. Open conformation = conformation of chromatin that makes it more accessible to transcription factors and RNA polymerase so transcription can happen b. Modifications Modification Whats Happening Alteration of DNA protein contacts - Sliding exposes DNA - Change in the relative positions of nucleosomes - Change in the spacing of nucleosomes over a large distance Alteration of the DNA path - DNA is pulled off nucleosome - Histone octamers are removed Remodeling of nucleosome core particle - Nucleosome dimer forms c. Cis-regulatory sequences i. Distal elements 1. Silencers = prevent transcription from occurring after binding a repressor 2. Enhancers = enhances the rate of transcription once bound by an activator ii. Proximal elements 1. Core promoters © Hannah Kennedy, Kent State University 7 4. Transcription Factors a. Key terminology i. up regulation = phenomenon in which transcription is greatly increased ii. down regulation = phenomenon in which transcription is decreased iii. domains = regions within TFs that have specific function (e.g. DNA binding function/provide binding site for small effector molecule) iv. motif = structure in which the domain or portion of it has a similar structure in many different proteins b. 2 categories of TFs i. general transcription factors = GTFs = required for the binding of RNA polymerase to the core promoter and its progression to the elongation stage; necessary for basal level transcription ii. regulator transcription factors = TFs that serve to regulate the rate of transcription of target genes 1. 2 protein complexes communicate RTFs effects a. transcription factor IID = TFIID = a GTF that binds to the TATA box and is needed to recruit RNA polymerase to the core promoter; activator proteins enhance its ability to increase transcription b. mediator = protein complex that mediates the interaction between RNA polymerase II and RTFs 5. Alternative Splicing a. Key terminology i. Alternative splicing = process in which certain pre-mRNAs can be spliced in more than 1 way to lead to polypeptides with different amino acid sequences ii. Constitutive exons = exons that are always found in the mature mRNA in all cell types iii. Alternative exons = exons that aren’t always found in mRNA after splicing; may change the function of a protein in a subtle way iv. Splicing factors = play a key role in the splice sites (e.g. SR proteins); key effects is to modulate the ability of the spliceosome to choose 5’ and 3’ splice sites; some inhibit ability of spliceosome to recognize splice site and some enhance spliceosome ability to recognize splice sites b. The purpose: to allow a protein to be specialized in a specific cell type c. Why it’s important: gene regulation, protein diversity, protein specialization Ch. 23.4—Medical Genetics and Cancer 6. 3 Characteristics common to all cancers a. originate in a single cell that undergoes genetic changes that accumulate b. Benign growth forms that is followed by additional genetic changes c. Cancerous cells become malignant (3 characteristics of malignant cells) i. Cell division occurs in unregulated way ii. Cells can invade healthy tissues (invasive) iii. Cells can migrate to other parts of the body and cause other tumors (metastatic) 7. Cancer as a genetic disease a. Key terminology i. Cancer = a disease characterized by uncontrolled proliferation of cells (i.e. normal fail-safe mechanisms that regulate cell growth and division have broken down) b. How we know that cancer is genetic—4 observations i. chromosol anomalies in cancer © Hannah Kennedy, Kent State University 8 1. Chromosomes with different morphology in a karyotype is characteristic of cancer (E.g. 9:22 translocation is responsible for Chronic Myeloid Leukemia) ii. Families where risk of cancer is transmitted as a trait iii. Carcinogens tend to be mutagens iv. Individuals with DNA repair deficiencies that have an increased risk of cancer c. Progression of cellular growth that leads to cancer—process i. Initial gene mutation converts normal cell to tumor cell ii. Tumor cell divides a lot to produce benign tumor iii. More genetic changes in the tumor cells lead to a malignant growth iv. Tumor cells invade surround tissues and some malignant cell metastasize by traveling through bloodstream to cause secondary tumors d. Cancer susceptibility genes increase the risk of cancer—3 ways i. Large number of genes are mutated in cancer cells that provide growth advantage for the cell population from which cancer developed ii. Abnormalities in chromosome structure and number 1. If tumor suppressor genes were on missing chromosome then function is lost, too 2. If there are extra chromosomes and they have proto-oncogenes, then the expression of those genes can be overactive iii. Tumor cells usually have chromosome that have translocations that can create fused genes or place 2 genes close together so that regulatory sequences of 1 affect expression of the other 8. Pedigrees a. Key terminology i. loss of heterozygosity = LOH = the loss of function of a normal allele when the other allele was already inactivated b. Mode of inheritance—2 questions to ask i. Autosomal or X-linked? 1. Autosomal is present in both sexes without any prevalent bias 2. X-liked appears from a mom to son inheritance pattern ii. Dominant or recessive? 1. Recessive isn’t present in every generation 2. Dominant doesn’t skip generations 9. Cell Cycle a. Key terminology i. Growth factors = signaling molecules that promote cell division; help regulate the cell cycle by binding to cell surface receptors and initiate cascade to lead to division ii. checkpoint proteins = proteins that detect genetic abnormalities like DNA breaks and improperly segregated chromosomes b. Commitment to divide based on several factors: optimal environmental conditions with sufficient nutrients and signaling molecules to coordinate cell division (i.e. growth factors such as EGF) c. Cyclins and CDKs: responsible for advancing a cell through the cell cycle i. Ex = activated G1 cyclin/CDK complex is needed to advance the cell from the G1 phase to the S phase d. 3 checkpoints in the cell cycle Checkpoint What’s Happening G1/S - Size and DNA integrity is monitored - Checkpoint proteins (e.g. p53) can © Hannah Kennedy, Kent State University 9 prevent formation of active cyclin/CDK complexes if DNA has damage G2/M - DNA synthesis and damage is monitored - Checkpoint proteins (e.g. p53) can prevent formation of active cyclin/CDK complexes if DNA has damage M - Spindle formation and attachment to kinetochores is monitored e. Checkpoint failure—leads to genetic instability i. Loss of checkpoint protein function can cause cancerous growth via unregulated cell division 10.Properties of cancer a. Key terminology i. genome maintenance = cellular mechanisms that prevent mutations from occurring and/or prevent mutant cells from surviving or dividing ii. Proto-oncogene = a normal, non-mutated gene that has the potential to become an oncogene iii. Oncogene = abnormally active gene that promotes cancerous growth b. 2 categories of genes i. tumor suppressor genes: prevents cancerous growth; loss of function mutation in it for cancer to occur (2 categories of genes) 1. genes that negatively regulate cell division 2. genes that maintain genome integrity (2 protein classes) a. checkpoint proteins b. proteins involved directly with DNA repair ii. proto-oncogenes: a normal, non-mutated gene that has the ability to become an oncogene; gain of function mutation for cancer to occur 11.Tumor suppressor genes a. First identified in Retinoblastoma i. Overview of Rb (retinoblastoma) protein: 1. it is inactivated by CDK/cyclin during G1/S checkpoint 2. it regulates the TF E2F that activates genes needed for cell cycle progression 3. if both Rb gene copies are inactive, then E2F is always active and uncontrolled cell division occurs ii. 2-hit model: 1. there are 2 copies of normal genes. Mutation occurs “first hit” and one gene is abnormal. There is still 1 functional gene at this point therefore we’re fine but not as protected. Second hit occurs, both genes become mutated, and growth will be uncontrolled © Hannah Kennedy, Kent State University 10 a. Those with hereditary form already have 1 mutant gene from 1 parent so they only need 1 more mutation in the other tumor- suppressor gene copy to develop retinoblastoma b. Those with non-inherited form of disease need 2 mutations in the same retinal cell b. Example: p53—a transcription factor critical for determining if a cell has DNA damage i. In normal cells: low p53 levels 1. Mdm2 removes p53 from the nucleus and leads to its degradation by the proteasome 2. acts as a negative regulator by interacting w GTFs to decrease the expression of other structural genes to inhibit the cell from dividing ii. In cells with DNA damage: p53 is activated as a TF via phosphorylation and acetylation 1. Mdm2 cannot bind to the modified p53 2. Inducing signal for the expression of the p53 gene is a ds DNA break iii. Activated p53 can employ 3 different pathways that prevent cell proliferation of those with DNA damage: 1. Cell tries to repair its DNA to prevent accumulation of mutations that activate oncogenes or inactive tumor suppressor genes 2. If cell is in process of dividing, it can arrest itself in the cell cycle so it has more time to repair DNA and avoid producing 2 mutant daughter cells a. This is done by p53 stimulating the expression of p21 that inhibits the cyclin/CDK protein complexes that are needed to progress from G1 phase to S phase 3. Apoptosis = programmed cell death a. Facilitated by caspases that digest cellular proteins c. 3 common ways that a tumor-suppressor gene can be lost i. Mutation can occur specifically within a tumor-suppressor gene to inactivate function 1. Ex = mutation can inactivate promoter or introduce early stop codon that prevent expression of functional protein ii. DNA methylation 1. inhibits the transcription of genes when in vicinity of promoter iii. Aneuploidy 1. chromosome loss contributes to cancer progression bc the chromosome that was lost carried 1 or more tumor suppressor genes 12.Oncogenes a. Examples of proteins that oncogenes encode in cell growth signaling pathways i. E.g. cyclins ii. Ex = c-myc 1. amplified in promyelocytic cell line; overexpression leads to transcriptional activation of genes that promote cell division iii. Ex = mutations that alter AA sequence of Ras protein cause functional abnormalities 1. Decrease ability of Ras protein to hydrolyze GTP © Hannah Kennedy, Kent State University 11 2. Increase rate of exchange of bound GDP for GTP a. Both result in greater amount of active GTP-bound form of Ras protein that keeps the signaling pathway on b. 4 ways that proto-oncogenes are turned into oncogenes Conversion What’s Happening Example Missense mutations Change in the AA sequence of Ras protein is transformed a proto-oncogene causes it to when glycine is changed to function abnormally valine Gene amplification Abnormal increase in the c-myc gene in leukemia copy number of the proto- oncogene that increases the amount of the encoded protein leading to malignancy Chromosomal translocation Piece of chromosome - Breakpoint in translocated to another chromosome 8 causes affects the expression of overexpression of c- genes at the breakpoint site myc gene - 9:22 translocation responsible for Chronic Myeloid Leukemia Viral integration Virus integrates into - papilloma virus chromosome and enhances promotes cervical the expression of close proto- cancer by blocking oncogenes and disrupts tumor suppressors chromosomes causing - HIV and Hepatitis B insertional mutagenesis and hepatocellular carcinoma 13.Mutagens and Carcinogens a. Key terminology i. Carcinogen = an environmental agent that causes cancer b. Ames test: to test for mutagens i. Ames test process: 1. Overall: a testing method that monitors whether an agent increases the mutation rate a. Suspected mutagen is mixed with rat liver extract and a strain of bacteria that cant synthesize histidine (mutagen may need activation by cell enzymes provided by rat liver extract) b. Bacteria plated on growth medium without histidine (bacteria not expected to grow on these plates but if a mutation occurs that allows it to synthesize histidine, it can grow) c. Mutation rate is estimated by counting the grown colonies on the media and compared with the number of bacterial cells that were originally streaked on the plate c. Potential carcinogens—diet i. Red meat and colon cancer are associated ii. High fat diets likely account for half of all tumors Ch. 24—Developmental Genetics 14.Pattern formation a. Key terminology © Hannah Kennedy, Kent State University 12 i. Morphogen = molecule that conveys positional information and promotes developmental changes over time; diffusible molecule that works in a concentration-dependent way to influence the developmental fate of the cell ii. Pattern = the spatial arrangement of different regions of the body due to the arrangement of cells and their specialization iii. Positional information = signals that cause a cell to follow a specific developmental pathway based on its position relative to other cells b. Positional information i. 4 ways a cell can respond to positional information 1. cell division—info can cause cell(s) to divide into groups of daughter cells 2. cell migration—cell(s) can migrate in a certain direction in the embryo 3. cell differentiation—cell(s) can differentiate into a specific cell type 4. cell death—necessary for the sculpting of tissues and organs ii. 3 mechanisms of positional information Mechanism What’s Happening Asymmetrical distribution of morphogens in - after fertilization the zygote subdivides an oocyte into smaller cells that have higher or lower concentrations of morphogens - polarity of ambryo occurs along anteroposterior & dorsoventral axis Asymmetrical synthesis and extracellular - Induction = the process by which a distribution of a morphogen in an embryo cell or group of cells governs the developmental fate of neighboring cells - Ex = Hedgehog protein in Drosophila is secreted from cells on posterior side of body segments to form a gradient from posterior to anterior region Cell-to-cell contact conveys positional - each cell has own surface receptors information that adhere to other cells of the ECM that is made of cell adhesions molecules - contacts made here can activate intracellular signal transduction pathways that lead to developmental changes 15.Animal development a. Key terminology i. bilaterians = most animals (and humans) that have left-right symmetry ii. determination = process in which groups of cells become destined to develop into specific structure and cell types; occurs before the structures and cell types have changes their morphologies b. Development happens in 4 overlapping stages i. Formation of body axes ii. Segmentation of the body 1. invertebrates: segments stay morphologically distinct 2. vertebrates: distinct segments are only apparent early on in development iii. determination of structures within the segments iv. cell differentiation c. Gene sets that control the phases of development Types of genes Description © Hannah Kennedy, Kent State University 13 Maternal effect genes - Expressed very early - Controls formation of body axes Segmentation genes - Results in segmentation Homeotic genes - Play central role in specifying the final identity of a body region - Controlled by gap genes and pair-rule genes - Encode TFs that activate genes to encode proteins that produce morphological characteristics of each segment - Homeotic mutants can result from something going wrong 16.Invertebrate development: Drosophila a. Key terminology b. Key processes i. (1) Determination = happens in interaction between a specific cell and the environment; process that determines the fate of the cell ii. (2) Differentiation = a much longer process in which the cells wire their specific features; grow their accents and their connections to these accents; not a set time-point iii. (3) Morphogenesis = development of entire organs; taking shape c. 7 developmental stages Developmental stage What’s Happening Oocyte—elongated cell with pre-established - fertilization takes place and zygote axes goes through nuclear divisions Syncytial blastoderm - resulting nuclei from nuclear divisions are scattered throughout yolk and majority of them migrate to periphery of cytoplasm Cellular blastoderm - individual cells are formed and portions of the cell membrane surround each nucleus - sheet of cells on the outside with yolk in the center - pole cells = cells found at the posterior end; germ cells that give rise to gametes Gastrula - Produces 3 cell layers: Ectoderm, mesoderm, endoderm - Boundaries form that divide the embryo into distinct segments Embryo Larva © Hannah Kennedy, Kent State University 14 Adult - 2 major axes: anteroposterior axis, dorseoventral axis - Gradients of cytoplasmic components define the anterior-posterior and dorsal-ventral axes of symmetry  action of the genome with the environmental will give rise to mRNA in the anterior portion of the egg that will up-regulate the formation of proteins that will compose the anterior of the organism d. Drosophila genes that play a role in pattern development Gene When it’s expressed Addtnl Info Example Maternal effect genes During oogenesis - Maternal effect - Bicoid: 1. —determines axes of = pattern of Bicoid development inheritance in mRNA which the given to genotype of the oocyte via mother nurse cells determines the 2. Gene phenotypic traits products of the offspring transferred from nurse cell to oocyte in oogenesis 3. Bicoid gene transcribed in nurse cells 4. Bicoid mRNA transported to 1 site of oocyte Segmentation genes— After fertilization (i.e. - 3 types of promote the type of zygotic gene) segment genes: subdivision of embryo gap, pair-rule, into segments and segment- polarity Homeotic genes— After fertilization - Antennaped determine the fate of ia complex particular segments - Bithorax complex e. Genetic hierarchy that leads to segmentation in Drosophila © Hannah Kennedy, Kent State University 15 i. Maternal effect gene products (e.g. bicoid mRNA) are deposited asymmetrically into oocyte—expressed during oogenesis 1. Establish the anteroposterior and dorsoventral axes 2. Activate gap genes ii. Zygotic genes—expressed after fertilization 1. Segmentation genes a. Gap genes act as genetic regulators of pair- rule genes 2. Homeotic genes iii. Gap genes and maternal effect genes activate the pair- rule genes 1. Defines the boundary of a parasegments 2. Regulate the expression of segment-polarity genes iv. Pair-rule gene products regulate the expression of segment-polarity genes that divide the embryo and define the anterior or posterior compartment of each parasegment 17.Vertebrate development a. Key terminology i. Hox complexes = groups of adjacent homeotic genes ii. Hox genes = encode transcription factors that regulate many diff genes; has allowed animals to develop more complex body plans and play a role in determining fates of segments along anteroposterior axis b. Evolutionary implication of Hox genes: increase in the # and change of pattern of Hox genes affect expression and morphology 18.Plant development a. ABC model: displays developmental homeotic genes in plants i. 3 genes: A, B, and C, contribute to the morphological development of plants 1. Gene A products: whorl 1, promote sepal formation 2. Gene A and B: whorl 2, promotes petal formation 3. Gene B and C: whorl 3, stamen formation 4. Gene C: whorl 4, carpel formation


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