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Lecture

BIOL 303 Study Questions Set 3
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Department
Biology
Course
BIOL 303
Professor
Dragana Miskovic
Semester
Fall

Description
BIOL 303 Study Questions Set 3 Key Concepts  Induction: one group of cells influences another group of cells to take on a different fate. Frequently between epithelium and mesenchyme cells (organs)  Paracrine factor: signal produced by inducer (soluble protein, peptides or glycoprotein).  Competence: ability to respond to a specific inductive signal. Needs to have an appropriate receptor.  Signal transduction: a signaling molecule activates a specific receptor protein on cell membrane, then a second messenger transmits signal into the cell.  Differentiation: The process by which an unspecialized cell becomes specialized into one of the many cell types that make up the body. Commitment: Describes a state in which a cell’s developmental fate has become  restricted even though it is not yet displaying overt changes in cellular biochemistry and function. The cell may not look different – but it is now more limited as to what it will become.  Determination  Specification  Autonomous specification  Conditional specification  Morphogen  Syncitial specification What is the difference between endocrine signaling and paracrine signaling?  Endocrine signaling: hormones in circulatory system that act along a great distance.  Paracrine signaling: localized production of paracrine factors (soluble proteins, peptides or glycoproteins) secreted into extracellular space. What is the difference between instructive and permissive induction?  Instructive: a signal from the inducing cell is necessary for initiating new gene expression in the responding cell.  Permissive: the responding tissue has already been specified and only needs an environment that allows for the expression of these traits (ex. Requires a substrate) What is an example of an inductive interaction that shows regional specificity and what is meant by genetic specificity?  Regional specificity: process by which different areas are identified in the development of the early embryo. The process by which the cells become specified differs between organisms.When cells from different regions of the dermis (mesenchyme) are recombined with the epidermis (epithelium), the type of cutaneous structure made by the epidermal epithelium is determined by the original source of the mesenchyme. Genetic specificity: the mesenchyme instructs the epithelium as to what genes to  activate, but that set of genes must be present in the genome. What is the difference between paracrine, juxtacrine and autocrine interactions?  Paracrine: proteins synthesized by one cell can diffuse over small distance to induce changes in neighboring cells.  Juxtacrine: cell membrane proteins on one cell surface interact with receptor proteins on adjacent cell surfaces.  Autocrine: the same cells that secrete paracrine factors also respond to them In what general way are signals associated with paracrine factors transduced into the receiving cell?  Receptors are transmembrane proteins.  When ligand binds they undergo a conformational change (tyrosine kinase).  Ligand binding can cause dimerization, autophosphorylation, and conformational change. What are the four main families of paracrine factors?  Fibroblast growth factor (FGF)  Hedgehog  Wnt (wingless)  Transforming growth factor (TGF-Beta) Looking at the regulation of the HEDGEHOG signaling pathway, what would be the overall outcome on the transcriptional response (up/down) of HEDGEHOG responsive genes when:  HEDGEHOG: protein; transmits information to embryonic cells required for proper development; key regulator of development in all bilaterians; gives rise to segmented body pattern  PATCHED: receptor  SMOOTHENED: protein, bound to patched  CUBITUS INTERUPTUS: protein that depends on smoothened  Hedgehog  Patched  Smoothened  Cubitus Interuptus  Transcription  Hedgehog paracrine factor is processed before being secreted and must be activated by binding to a molecule of cholesterol. o HEDGEHOG binds PATCHED and the conformation of PATCHED changes o This relieves the inhibition of SMOOTHENED o Activation of SMOOTHENED releases CUBITUS INTERUPTUS and CI is cleaved o Free CI protein enters nucleus o Nuclear CI binds Cubitis Binding Protein and activates target genes a) The function of PATCHED is eliminated by a mutation  If PATCHED receptor cannot bind HEDGEHOG protein, then PATCHED represses SMOOTHENED. Without SMOOTHENED activity the CUBITUS INTERUPTUS protein remains bound to microtubules COS2 and FUSED, where it is cleaved by PKA and SLIMB. One of the cleaved products is a nuclear transcription repressor and no transcription of HEDGEHOG responsive genes takes place. b) Function of CUBITUS INTERUPTUS is reduced by mutation  CUBITUS INTERUPTUS cannot be freed form microtubules and will not be able to enter nucleus and bind to CBP protein that will activate HEDGEHOG genes. c) Post-translational modification of HEDGEHOG is prevented  The pathway will not go forth. HEDGEHOG requires to be bound to a molecule of cholesterol to be activated. d) Cells are treated with a drug that increases the activity of SMOOTHENED.  More CI will be cleaved and free to enter nucleus to bind to CBP and create HEDGEHOG genes. In general, Notch signaling is different from other signaling pathways because it is very sensitive to the total amount of Notch receptor (called dosage sensitivity). Looking at the mechanism of Notch signal transduction, can you suggest a reason why this would be so?  Notch is a receptor that binds Delta. Notch protein undergoes a conformational change upon binding. Notch becomes a substrate for presenilin-1 protein. The cleaved portion of Notch is localized to the nucleus and activates transcription factor CSL.  Notch spans the cell membrane. Receptor is triggered via direct-cell contact, where the transmembrane protein of the other cell binds to the Notch receptor.  Notch: example of juxtacrine interaction (cell membrane proteins on one cell surface interact with receptor proteins on adjacent cell surfaces). No diffusion of inducer because the ligand and receptor are both transmembrane proteins.  There is no amplification step during signal transduction, unlike other pathways. Each activated Notch receptor molecule is consumed during signaling, yielding one Notch intracellular domain (from receptor, is cleaved upon binding a ligand). This suggests there is a stoichiometric relationship between input and output (ie one in, one out) and signal strength is important for generating the appropriate cellular response. Both haploinefficiency (only one functional copy of the gene does not produce enough gene product to bring about a wild-type phenotype) and extra copies can produce this effect. Briefly outli
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