Honors ~ Cells & insulin and cell communication 1314
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The document discusses cell signaling and cell structure. It includes diagrams of cell organelles like the endoplasmic reticulum, nucleus, and mitochondria. It also covers topics such as osmosis, cell transport mechanisms like diffusion and active transport, and cell signaling pathways. Diagrams show G protein-coupled receptor signaling and second messenger systems and how they lead to cellular responses. The document also discusses mating in yeast cells and the formation of shmoo projections in response to mating pheromones.
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Honors ~ Cells & insulin and cell communication 1314
- 1. Cells: Honors Biology ~ Edgar
- 3. Counting Guidelines • Cells Should not be overlapping. • Cells should be uniformly distributed • You need to count 100 cells to be statistically significant. • Where to Count – no bias.
- 4. Which Cells to Count
- 11. Figure 6.8a ENDOPLASMIC RETICULUM (ER) Flagellum Rough Smooth ER ER Nuclear envelope NUCLEUS Nucleolus Chromatin Centrosome Plasma membrane CYTOSKELETON: Microfilaments Intermediate filaments Microtubules Ribosomes Microvilli Golgi apparatus Peroxisome Mitochondrion Lysosome
- 12. Figure 6.8c Nuclear envelope NUCLEUS Nucleolus Chromatin Rough endoplasmic reticulum Smooth endoplasmic reticulum Ribosomes Central vacuole Golgi apparatus Microfilaments Intermediate filaments Microtubules Mitochondrion Peroxisome Chloroplast Plasma membrane Cell wall Wall of adjacent cell Plasmodesmata CYTOSKELETON
- 13. Cell Biology and Diabetes
- 14. Insulin
- 21. Red arrows indicate Beta Cells
- 52. Figure 11.5a Local signaling Electrical signal along nerve cell triggers release of neurotransmitter. Target cell Secreting cell Local regulator diffuses through extracellular fluid. (a) Paracrine signaling Neurotransmitter diffuses across synapse. Secretory vesicle Target cell is stimulated. (b) Synaptic signaling
- 53. Figure 11.5b Long-distance signaling Endocrine cell Blood vessel Hormone travels in bloodstream. Target cell specifically binds hormone. (c) Endocrine (hormonal) signaling
- 55. Figure 11.6-1 EXTRACELLULAR FLUID 1 Reception Receptor Signaling molecule CYTOPLASM Plasma membrane
- 56. Figure 11.6-2 EXTRACELLULAR FLUID 1 Reception CYTOPLASM Plasma membrane 2 Transduction Receptor Relay molecules in a signal transduction pathway Signaling molecule
- 57. Figure 11.6-3 EXTRACELLULAR FLUID 1 Reception CYTOPLASM Plasma membrane 2 Transduction 3 Response Receptor Relay molecules in a signal transduction pathway Signaling molecule Activation of cellular response
- 62. Igf-1
- 64. Types of Cell Receptors
- 67. GCPR on Beta Cells
- 69. Figure 11.7c Signaling molecule (ligand) Ligand-binding site Signaling molecule α helix in the membrane Tyr Tyr Tyr CYTOPLASM Tyr Tyr Tyrosines Tyr Tyr 1 Tyr Tyr Tyr Tyr Tyr Tyr Tyr Receptor tyrosine kinase proteins (inactive monomers) Tyr Tyr Tyr Tyr Dimer 2 Activated relay proteins Tyr P Tyr Tyr P Tyr Tyr P Tyr ATP Activated tyrosine kinase regions (unphosphorylated dimer) 6 ADP Fully activated receptor tyrosine kinase (phosphorylated dimer) 4 Tyr P P Tyr Tyr P 6 Tyr P P Tyr Tyr P Tyr P Tyr Tyr P Tyr 3 Tyr Tyr P Inactive relay proteins Cellular response 1 Cellular response 2
- 70. Insulin Receptor tyrosine kinase receptor
- 74. Figure 11.7d 1 Signaling molecule (ligand) 3 2 Gate closed Ions Plasma Ligand-gated membrane ion channel receptor Gate closed Gate open Cellular response
- 77. Figure 11.10 Signaling molecule Receptor Activated relay molecule Inactive protein kinase 1 ATP P de ca Inactive protein kinase 3 s ca PP n Active protein kinase 2 tio Pi ADP yla Inactive protein kinase 2 or ph os Ph Active protein kinase 1 ATP ADP Pi Active protein kinase 3 PP Inactive protein P ATP P ADP Pi PP Active protein Cellular response
- 82. Figure 11.12 First messenger (signaling molecule such as epinephrine) Adenylyl cyclase G protein G protein-coupled receptor GTP ATP cAMP Second messenger Protein kinase A Cellular responses
- 84. Figure 11.16 Reception Binding of epinephrine to G protein-coupled receptor (1 molecule) Transduction Inactive G protein Active G protein (102 molecules) Inactive adenylyl cyclase Active adenylyl cyclase (102) ATP Cyclic AMP (104) Inactive protein kinase A Active protein kinase A (104) Inactive phosphorylase kinase Active phosphorylase kinase (10 5) Inactive glycogen phosphorylase Active glycogen phosphorylase (10 6) Response Glycogen Glucose 1-phosphate (108 molecules)
- 85. Figure 11.13 EXTRACELLULAR FLUID ATP Plasma membrane Ca2+ pump Mitochondrion Nucleus CYTOSOL Ca2+ pump ATP Key High [Ca2+ ] Ca2+ pump Endoplasmic reticulum (ER) Low [Ca2+ ]
- 87. Figure 11.14-1 EXTRACELLULAR FLUID Signaling molecule (first messenger) G protein DAG GTP G protein-coupled receptor IP3-gated calcium channel Endoplasmic reticulum (ER) CYTOSOL Ca2+ Phospholipase C PIP2 IP3 (second messenger)
- 88. Figure 11.14-2 EXTRACELLULAR FLUID Signaling molecule (first messenger) G protein DAG GTP G protein-coupled receptor Phospholipase C IP3 (second messenger) IP3-gated calcium channel Endoplasmic reticulum (ER) CYTOSOL PIP2 Ca2+ Ca2+ (second messenger)
- 89. Figure 11.14-3 EXTRACELLULAR FLUID Signaling molecule (first messenger) G protein DAG GTP G protein-coupled receptor Phospholipase C PIP2 IP3 (second messenger) IP3-gated calcium channel Endoplasmic reticulum (ER) CYTOSOL Ca 2+ Ca2+ (second messenger) Various proteins activated Cellular responses
- 90. Diabetes
- 95. Looking good. The pancreas of a mouse after it was transplanted with human beta cells (left) looks similar to that of an animal that produces insulin normally (right). CREDIT: Narushima et al., Nature Biotechnology Brimming with b's. Newfound cells in the pancreas give rise to neurons (red) and insulinproducing b cells (green). CREDIT: SEABERG ET AL., NATURE BIOTECHNOLOGY The full picture. Human ES cells can eventually give rise to cells that resemble pancreatic beta cells (labeled β).
- 96. Cell Membranes and Transport Honors Biology ~ Edgar
- 101. Glucose, Starch, IKI, Water
- 105. Osmosis
- 106. Osmosis
- 108. Concept Check • If a Paramecium were to swim from a hypotonic environment to an isotonic one, would the activity of its contractile vacuole increase or decrease? Why?
- 111. Concept Check • This diagram represents osmosis of water across a semipermeable membrane. The U-tube on the right shows the results of the osmosis. What could you do to level the solutions in the two sides of the right hand U-tube? a) b) c) d) Add more water to the left hand side. Add more water to the right hand side. Add more solute to the left hand side. Add more solute to the right hand side.
- 112. Answer •This diagram represents osmosis of water across a semipermeable membrane. The U-tube on the right shows the results of the osmosis. What could you do to level the solutions in the two sides of the right hand U-tube? c) Add more solute to the left hand side.
- 119. Jmol
- 120. Harvard BioVisions
- 128. Vegetables in Sucrose Solutions Percent Change in Mass (%) 30.00 20.00 10.00 Beet 0.00 Potato Carrot -10.00 -20.00 -30.00 0 0.2 0.4 0.6 0.8 1 Sucrose Concentration (Molarity) 1.2
- 129. Figure 11.2 α factor Receptor 1 Exchange of mating factors α a a factor Yeast cell, Yeast cell, mating type a mating type α 2 Mating α a 3 New a/α cell a/α
- 130. Figure 11.17 RESULTS CONCLUSION 1 Mating factor activates receptor. ∆formin ∆Fus3 Wild type (with shmoos) Mating factor G protein-coupled Shmoo projection forming receptor Formin P Fus3 GDP GTP 2 G protein binds GTP and becomes activated. Fus3 Actin subunit P Phosphorylation cascade Fus3 Formin Formin P 4 Fus3 phosphorylates formin, activating it. P 3 Phosphorylation cascade activates Fus3, which moves to plasma membrane. Microfilament 5 Formin initiates growth of microfilaments that form the shmoo projections.
Editor's Notes
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- The process by which insulin is released from beta cells, in response to changes in blood glucose concentration, is a complex and interesting mechanism that illustrates the intricate nature of insulin regulation. Type 2 glucose transporters (GLUT2) mediate the entry of glucose into beta cells (see panel 2). As the raw fuel for glycolysis, the universal energy-producing pathway, glucose is phosphorylated by the rate-limiting enzyme glucokinase. This modified glucose becomes effectively trapped within the beta cells and is further metabolized to create ATP, the central energy molecule. The increased ATP:ADP ratio causes the ATP-gated potassium channels in the cellular membrane to close up, preventing potassium ions from being shunted across the cell membrane. The ensuing rise in positive charge inside the cell, due to the increased concentration of potassium ions, leads to depolarization of the cell. The net effect is the activation of voltage-gated calcium channels, which transport calcium ions into the cell. The brisk increase in intracellular calcium concentrations triggers export of the insulin-storing granules by a process known as exocytosis. The ultimate result is the export of insulin from beta cells and its diffusion into nearby blood vessels. Extensive vascular capacity of surrounding pancreatic islets ensures the prompt diffusion of insulin (and glucose) between beta cells and blood vessels. Insulin release is a biphasic process. The initial amount of insulin released upon glucose absorption is dependent on the amounts available in storage. Once depleted, a second phase of insulin release is initiated. This latter release is prolonged since insulin has to be synthesized, processed, and secreted for the duration of the increase of blood glucose. Furthermore, beta cells also have to regenerate the stores of insulin initially depleted in the fast response phase.
- Figure 11.5 Local and long-distance cell signaling by secreted molecules in animals.
- Figure 11.5 Local and long-distance cell signaling by secreted molecules in animals.
- Figure 11.6 Overview of cell signaling.
- Figure 11.6 Overview of cell signaling.
- Figure 11.6 Overview of cell signaling.
- A single gene may explain the vast size difference between that tiny terrier yapping in the park and the massive mastiff ignoring the din. Nate Sutter, a geneticist at the National Human Genome Research Institute in Bethesda, Maryland, wanted to know the reason why big dogs, such as Irish wolfhounds, can grow up to 50 times larger than other members of their own species, such as chihuahuas. So he started out looking at large and small dogs of one breed — the Portuguese water dog. Scientists on the team took X-rays of 500 Portuguese water dogs and made 91 measurements of their skeletons. Based on these data, the researchers classified the water dogs as either big or small for their own breed. They then looked for differences in DNA between the large and small water dogs. This is a relatively easy job: a consortium of scientists including Sutter published the DNA sequence of the dog genome last December, and have mapped out the places where there is a lot of variation between individuals in a given breed. There are fewer of these places of variation in purebred dogs than there are in humans. The team found that one of the few differences in these Portuguese water dogs occurred in a gene called 'insulin-like growth factor 1', or Igf-1. This is one of many genes already known to influence the size of mice: when Igf-1 is knocked out, the animals grow up to be mini-mice. So the team wondered whether this gene was responsible for dog body size. Great pomeranians? To answer this question, scientists closely analysed the Igf-1 genes in 75 Portuguese water dogs and 350 other dogs of very large and very small breeds — from pomeranians and Yorkshire terriers up to great Danes and St Bernards. They also examined the gene in wild dogs, such as wolves and foxes, who are distantly related to domestic dogs. They found that almost all of the 18 small breeds carried the identical variant of the gene as small Portuguese water dogs. But almost none of the 15 giant breeds carried this gene variant. That suggested that the gene plays a major role in controlling dog body size, Sutter said on 11 October at the annual meeting of the American Society of Human Genetics in New Orleans, Louisiana. If researchers want to make a giant chihuahua, they now know where to start. The gene seems to work by setting how much of the growth factor dogs make. In Portuguese water dogs, smaller animals make less of the growth factor than big ones. The 'small' version of Igf-1 seems to have formed long ago, Sutter says. When humans began breeding tiny dogs, they inadvertently selected for this version of the gene, and over time the breeding process fixed the 'small' variant into tiny dog breeds. Man's best friend The study proves how useful genetic studies in dogs can be, Sutter says. Because dog breeders know the history of individual dogs in a breed, and because the dogs are purebred — meaning they have lost a lot of their genetic variation — it is easier to uncover the genetic causes of traits such as body size than it is in people. ADVERTISEMENT Other members of Sutter's group, led by Elaine Ostrander, are also looking for genes that cause diseases including cancer. Sutter says he hopes that they will find similar success. "The power in dog populations is that they can deliver a simple genetic story about a precise genetic trait," Sutter says. "I think we're also going to find this with other complex traits Action Its primary action is mediated by binding to specific IGF receptors present on many cell types in many tissues. The signal is transduced by intracellular events. IGF-1 is one of the most potent natural activators of the AKT signaling pathway, a stimulator of cell growth and multiplication and a potent inhibitor of programmed cell death. Almost every cell in the human body is affected by IGF-1, especially cells in muscle, cartilage, bone, liver, kidney, nerves, skin, and lungs. In addition to the insulin-like effects, IGF-1 can also regulate cell growth and development, especially in nerve cells, as well as cellular DNA synthesis. [edit] IGF-2 and Insulin; related growth factors IGF-1 is closely related to a second protein called "IGF-2". IGF-2 also binds the IGF-1 Receptor. However, IGF-2 alone binds a receptor called the "IGF II Receptor" (also called the Mannose-6 phosphate receptor). The insulin growth factor-II receptor (IGF2R) lacks signal transduction capacity, and its main role is to act as a sink for IGF-2 and make less IGF-2 available for binding with IGF-1R. As the name "insulin-like growth factor 1" implies, IGF-1 is structurally related to insulin, and is even capable of binding the insulin receptor, albeit at lower affinity than insulin.
- Figure 11.7 Exploring: Cell-Surface Transmembrane Receptors
- Figure 11.7 Exploring: Cell-Surface Transmembrane Receptors
- Figure 11.10 A phosphorylation cascade.
- Figure 11.12 cAMP as a second messenger in a G protein signaling pathway.
- Figure 11.16 Cytoplasmic response to a signal: the stimulation of glycogen breakdown by epinephrine.
- Figure 11.13 The maintenance of calcium ion concentrations in an animal cell.
- Figure 11.14 Calcium and IP3 in signaling pathways.
- Figure 11.14 Calcium and IP3 in signaling pathways.
- Figure 11.14 Calcium and IP3 in signaling pathways.
- There is promising news today for those who hope to turn the potential of undifferentiated stem cells into medical miracles: Researchers are reporting a way to produce insulin-producing cells from mouse embryonic stem cells. Millions of diabetes patients could benefit if researchers can achieve such alchemy with human cells. ILLUSTRATION: CAMERON SLAYDEN Doctors have reported promising results in transplanting pancreatic cells from cadavers into diabetic patients, enabling a handful of recipients to stop insulin injections indefinitely. But the demand for cells is far greater than the supply, and an unlimited source of cells that could produce insulin would be a hot commodity. So far, success at growing such cells from stem cells has been limited. Ron McKay and his colleagues at the National Institute of Neurological Disease and Stroke in Bethesda, Maryland, usually focus on brain development, but they were intrigued by recent papers reporting that some pancreas cells express nestin, a protein typical of developing neural cells. The scientists already knew how to encourage mouse embryonic stem cells to express nestin, and they wondered if they could coax their nestin-positive cells to take on more characteristics of pancreas cells. When they briefly exposed nestin-positive cells to a growth factor, the cells differentiated not only into neural cells but also into clusters that resemble the insulin-producing islets in the pancreas. The clusters' inner cells produced insulin, while outer cells produced glucagon and somatostatin, two proteins typical of pancreas cells, the team reports in a paper published online today by Science. "The percentage of cells that become insulin positive is remarkable and way above what others have reported," says developmental biologist Palle Serup, who studies pancreas development at the Hagedorn Research Institute in Gentofte, Denmark. Yet important caveats remain. The clusters produce only about 2% as much insulin as normal islets and failed to make insulin in response to a glucose level that typically triggers a response in normal cells. That does not discourage researchers like molecular biologist Ken Zaret of the Fox Chase Cancer Center in Philadelphia. "The glass is 1/50th full," says Zaret, who predicts that refinements in the culture technique or drug manipulations will boost insulin production. Stem Cell Letdown in Pancreas Insulin-producing cells in the pancreas of adult mice apparently don't develop from stem cells, an experiment has shown. Instead, they derive from the reproduction of existing cells--the kind that are destroyed in type I diabetes. The find, published in this week's issue of Nature, suggests that if scientists can find ways to boost the proliferation of these cells it might be useful for treating type I diabetes. In type I diabetes, a misdirected immune system apparently attacks and kills pancreatic islet cells, called B cells. These cells respond to glucose levels in the blood by producing insulin. When they die, patients must inject themselves with insulin. Preliminary studies have suggested that transplanting donor B cells into patients can free recipients of the need to inject insulin. But the supply of transplantable cells is limited; each transplant requires cells from several cadavers. Scientists hoping to find a plentiful source for B cells have been searching for pancreatic stem cells. In an effort to pin down the source of new B cells in the body, Douglas Melton of Harvard University and his colleagues designed transgenic mice in which insulin-producing cells could be prompted to produce a protein, called HPAP, that is detectable with a blue stain. When the mice were 6 to 8 weeks old, the team turned on the HPAP gene. (This labeled about a third of the insulin-producing B cells.) Once the HPAP gene is turned on, B cells will pass the gene on to any daughter cells. But if new B cells instead come from stem cells, which presumably don't make insulin, they should not be labeled by the stain, the team reasoned. The scientists allowed some of the mice to live up to 12 months--midlife for a mouse--before sacrificing them and examining the pancreas. If stem cells had been active, they would have produced unstained B cells, upping their abundance relative to the stained cells. But instead, the percentage of blue stained cells was higher in the year-old mice than in the 6-week-old mice. This suggests that B cells replicate themselves, Melton's team says, and that the pancreas is unlikely to harbor stem cells that produce large numbers of new B cells. "The experiment is an elegant demonstration that B cells can themselves proliferate," says Ronald McKay of National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. The trick now is finding the factors that regulate that proliferation of B cells so scientists might be able to grow the cells in culture, he says.
- Figure 11.2 Communication between mating yeast cells.
- Figure 11.17 INQUIRY: How do signals induce directional cell growth during mating in yeast?