Presentation on theme: "THE CYTOSKELETON AND RELATED STRUCTURES"— Presentation transcript:
1THE CYTOSKELETON AND RELATED STRUCTURES The cell’s internal skeleton helps organize its structure and activitiesA network of protein fibers make up the cytoskeleton.Actin subunitMicrofilament7 nmFibrous subunits10 nmIntermediate filamentMicrotubule25 nmTubulin subunit
2Microfilaments of actin Intermediate filaments Enable cells to change shape and moveIntermediate filamentsReinforce the cell and anchor cer tain organellesMicrotubules give the cell rigidityAnd provide anchors for organelles and act as tracks for organelle movement
3A typical plant cell has some structures that an animal cell lacks Such as chloroplasts and a rigid cell wallCentral vacuoleNot in animal cellsChloroplastCell wallGolgi apparatusNucleusMicrotubuleCytoskeletonIntermediate filamentMicrofilamentRibosomesSmooth endoplasmic reticulumMitochondrionPeroxisomePlasma membraneRough endoplasmic reticulumFigure 4.4B
4Plant cellsAre suppor ted by rigid cell walls made largely of celluloseConnect by plasmodesmata, which are connecting channelsPlasma membraneCytoplasmPlasmodesmataVacuoleLayers of one plant cell wallWalls of two adjacent plantcellsFigure 4.18A
5Tight junctions can bind cells together into leakproof sheets Anchoring junctions link animal cells into strong tissuesGap junctions allow substances to flow from cell to cellAnchoring junctionTight junctionsGap junctionsExtracellular matrixSpace between cellsPlasma membranes of adjacent cellsFigure 4.18B
7Cystic Fibrosis and the Cell Membrane Cystic fibrosis (CF) is caused by a salt imbalance, making mucus in the lungs and digestive system extremely thick.Caused by recessive gene; about 20% of us are carriersSeveral new treatments, including a healthy gene introduced into the lungs in a nasal spray, target the illness at the cellular source.Source:
8Adrenoleukodystrophy (ALD) and Peroxisomes Cause: peroxisomes lacked the second most abundant protein in the outer membrane of this organelle.Normally, the missing protein (a chaperone protein) transports an enzyme into the peroxisome.Without the enzyme, fatty acids builds up in cells in the brain and spinal cord, eventually myelin is depleted (vital for nerve transmission). Death comes in a few years.For many sufferers of ALD, eating a type of triglyceride from rapeseed (canola) oil slows buildup of the very long chain fatty acids for a few years, stalling symptoms. But the treatment eventually impairs blood clotting and other vital functions, and fails to halt the progression of the illness.
10Tay-Sachs Disease and Lysosomes More common in some ethnic communities, a mutation of an enzyme in lysosomesIn eyes, a telltale cherry red spot indicates the illnessthe lysosomes, tiny enzyme-filled sacs, swell to huge proportions.These lysosomes lack one of the forty types of lysosomal enzymes, results in built up fatty material on nerve cells.Sadly and commonly, the nervous system continues to fail, and paralysis , then death before the age of four.
12Cystic Fibrosis & the Rough ER a prominent example of a disease caused by misfolded proteins.CF is an ultimately fatal inherited disorder in which the lack of a specific type of plasma membrane chloride channel, the cystic fibrosis transmembrane regulator (CFTR), causes the accumulation of a thick mucus that compromises several organs, most notably the lungs and pancreas.The misfolded CFTR protein becomes trapped within the ER and is subsequently degraded.Source:
13ER stressinduced by a variety of conditions such as proteinaggregation, Ca2 depletion, glucose deprivation, or fatty acidoverload, can result in severe cell dysfunction or death.It is an important feature of such neuro-degenerative conditions as Alzheimer’s, Huntington’s, and Parkinson’s diseases, as well as heart disease and diabetes.
15GOLGI APPARATUSThe most commonly recognized Golgi-linked diseases are a group of 15 congenital disorders of glycosylation (CDG).Caused by mutations in genes that encode glycosylation enzymes or glycosylation-linked transport proteinsa CDG is usually lethal by the age of 2.Symptoms include mental retardation, seizures, and liver disease.
16Nuclear Membrane problems defects in the nuclear envelope occur in the genes that code for lamin, a cytoskeletal component of the nuclear lamina, and emerin, an inner membrane protein.
171. Progeriaa fatal childhood disease characterized by premature aging of the musculoskeletal and cardiovascular systemsHas been linked to a specific mutation in the lamin A gene.
182. Emery-Dreifuss muscular dystrophy caused by the absence or mutation of the gene that codes for emerinSymptoms include:a fragile nuclear membranealtered regulation of DNA replication and transcriptionand low tolerance to mechanical stress.
19Lysosomes & Peroxisomes lysosomal storage diseases (LSD)caused by the absence of one or more lysosomal enzymesExamples:Tay-Sachs and Gaucher’s, as well as Pompe’s disease (glycogen storage disease type II), are caused by the absence of a single enzyme. Death occurs in early childhood.In I-cell disease, the import of all lysosomal enzymes into lysosomes in certain organs is defective. In affected cells, the enzymes are instead secreted into the extracellular matrix. Symptoms include mental deterioration, heart disease, and respiratory failure.
20Mitochondrial problems High rates of mutation, since it is an ancient bacteriumMutation in proteins that guide mitochondrial division create dissimilar daughter mitochondriaThis increases risk of inheriting mutations that are harmful to mitochondrial function.Examples: exercise intolerance, chronic fatigueExamples: diabetes, Parkinson’s, Alzheimer’s
22Mitochondria & Cancer?In 1998, a link between colorectal cancer and somatic mitochondrial mutations was established by Polyak and colleagues.These researchers cultured colorectal cancer cells taken from the tumors of 10 colorectal cancer patients, and found significant mitochondrial mutations not present in nearby tissues samples.Conclusion: perhaps mutated mitchondrial enable enhanced ATP production needed by cancer cells for fast reproduction?
23MtDNA accumulates mutations rapidly mtDNA accumulates mutations approximately 10 times faster than nuclear DNA.Why?:repair mechanisms present in the nucleus are absent in mitochondriamitochondria produce oxygen free radicals that can oxidize DNA and RNA (usually producing mutations)mtDNA lacks histones proteins , which are thought to protect DNA from damage
24The Inner Life of the Cell The Harvard Cell VideoThe XVIVO Version of the Video