Test Ch.20 Flashcards
Define tissues and name four major tissue types in animals.
Tissues are the cooperative assembly of cells and extracellular matrix (ECM) that form a functional unit.
Four major tissue types in animals:
Connective tissue
Epithelial tissue
Muscular tissue
Nervous tissue
Describe the overall structure and function of connective tissues.
Structure:
Connective tissues have lots of ECM and fewer cells.
Function:
The ECM carries the mechanical load (provides strength, support, fills space).
Extracellular matrix (ECM) is made inside connective tissue cells (fibroblasts or osteoblasts) and secreted into the extracellular space
ECM mostly made up of collagen protein
Forms fibrils and fibers with high tensile strength
ECM also contains gels of proteins and polysaccharides that fill spaces and resist compression.
All secreted by fibroblasts
Examples: Tendons, cartilage, dermis of skin, bone.
Describe the assembly and function of collagen including cell types that make collagen
Assembly:
Collagen is first secreted as procollagen by cells like fibroblasts (or osteoblasts in bone).
Procollagen proteinase cleaves procollagen → forming mature collagen.
Collagen molecules self-assemble into fibrils and fibers with high tensile strength.
Fibroblasts crawl along fibrils to organize the final structure.
Function:
Provides tensile strength to tissues, preventing tearing.
Describe how cells are attached to the extracellular matrix and the role of integrins and fibronectin.
Fibronectin:
A bridge protein that binds collagen in the ECM.
Integrins:
Transmembrane receptor proteins on the cell surface.
Bind fibronectin outside the cell and connect to actin filaments inside via adaptor proteins.
Function:
Allows cells to attach stably or move dynamically through the ECM.
Describe the structure and function of epithelial tissue.
Structure:
Sheets of tightly packed cells.
Cover body surfaces and line internal cavities.
Attachment:
Epithelial cells attach to a thin layer of connective tissue called the basal lamina (using integrins in hemidesmosomes).
Function:
Forms barriers, protects underlying structures, controls permeability.
Discuss the role of the basal lamina, cadherins, and the cytoskeleton in epithelial cell stability and tissue structure.
-Basal lamina:
A thin ECM layer that anchors epithelial sheets to connective tissue.
-Cadherins:
Cell adhesion proteins that connect neighboring cells by homophilic binding (like-to-like binding).
Connect to actin (via adherens junctions) or intermediate filaments (via desmosomes).
-Cytoskeleton:
Provides mechanical strength and resistance to stress.
Actin + intermediate filaments = internal “scaffold” linking cells together.
Distinguish between the structure and function of 5 types of cell junctions found in animal cells.
Look on google docs
Distinguish between stem cells, precursor cells, and terminally differentiated cells and describe their roles in tissue function and renewal.
-Stem cells:
Can self-renew and differentiate into multiple cell types.
-Precursor cells:
Derived from stem cells.
Limited ability to divide and differentiate into specific cell types.
-Terminally differentiated cells:
Fully specialized cells (e.g., absorptive cells, goblet cells).
No division; carry out tissue functions until they die.
Discuss cell behaviors that help maintain tissue organization.
-Cell communication:
Signals control when cells divide, differentiate, or die.
-Selective adhesion:
Cells preferentially adhere to specific neighbors using cadherins.
-Cell memory:
Maintains specialized gene expression patterns even through divisions.
➡️ Violations of these behaviors can lead to cancer.
Distinguish between and describe the roles of oncogenes and tumor suppressor genes in cancer formation.
-Oncogenes:
~Mutated forms of proto-oncogenes (genes that normally promote cell division/growth).
~Gain-of-function mutations (only one mutated copy needed).
~Cause cells to divide uncontrollably.
-Tumor suppressor genes:
~Normally inhibit cell growth or promote apoptosis.
~Loss-of-function mutations (both copies must be mutated).
~Fail to stop abnormal growth.
Describe the selective advantages cancer cells gain over normal cells and how these advantages arise.
Advantages cancer cells develop:
Reduced dependence on growth signals (mutated Ras, Rb).
Resistance to apoptosis (e.g., p53 mutation).
Unlimited divisions (activate telomerase).
Genetic instability (mutated DNA repair genes).
Ability to invade (lose cadherins/integrins).
Angiogenesis promotion (new blood vessels for nutrients).
Tolerance to low oxygen (use glycolysis/fermentation).
Arise by accumulating multiple mutations (usually 5–8 key mutations are needed).
Identify and discuss steps in cancer cell production that can or cannot be targeted for drug therapies.
-Targetable steps:
~Overactive receptor tyrosine kinases (e.g., Herceptin for HER2 breast cancer).
~Overactive kinases (e.g., Gleevec for BCR-ABL in leukemia).
~Blood vessel formation (anti-angiogenesis drugs).
~Use of immunotherapy (e.g., Keytruda targets abnormal surface markers).
-Hard-to-target steps:
~Random genetic mutations.
~Metastasis (cell invasion into new tissues).
~General chromosomal instability.
