Honors - Cells, insulin, signaling and membranes 1213
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Honors - Cells, insulin, signaling and membranes 1213
- 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
- 14. Figure 6.8a ENDOPLASMIC RETICULUM (ER) Nuclear Rough Smooth envelope Flagellum ER ER NUCLEUS Nucleolus Chromatin Centrosome Plasma membrane CYTOSKELETON: Microfilaments Intermediate filaments Microtubules Ribosomes Microvilli Golgi apparatus Peroxisome Mitochondrion Lysosome
- 15. Figure 6.8b Animal Cells Fungal Cells 1 µm Parent 10 µm cell Cell wall Buds Vacuole Cell 5 µm Nucleus Nucleus Nucleolus Mitochondrion Human cells from lining Yeast cells budding A single yeast cell of uterus (colorized TEM) (colorized SEM) (colorized TEM)
- 16. Figure 6.8ba Animal Cells 10 µm Cell Nucleus Nucleolus Human cells from lining of uterus (colorized TEM)
- 17. Figure 6.8bb Fungal Cells Parent cell Buds 5 µm Yeast cells budding (colorized SEM)
- 18. Figure 6.8bc 1 µm Cell wall Vacuole Nucleus Mitochondrion A single yeast cell (colorized TEM)
- 19. Figure 6.8c Nuclear Rough envelope endoplasmic NUCLEUS reticulum Smooth Nucleolus endoplasmic reticulum Chromatin Ribosomes Central vacuole Golgi apparatus Microfilaments Intermediate CYTOSKELETON filaments Microtubules Mitochondrion Peroxisome Plasma membrane Chloroplast Cell wall Plasmodesmata Wall of adjacent cell
- 20. Figure 6.8d Plant Cells Protistan Cells Flagella 1 µm Cell 5 µm 8 µm Cell wall Nucleus Chloroplast Nucleolus Mitochondrion Vacuole Nucleus Nucleolus Chloroplast Chlamydomonas Cells from duckweed (colorized SEM) Cell wall (colorized TEM) Chlamydomonas (colorized TEM)
- 21. Figure 6.8da Plant Cells Cell 5 µm Cell wall Chloroplast Mitochondrion Nucleus Nucleolus Cells from duckweed (colorized TEM)
- 22. Figure 6.8db Protistan Cells 8 µm Chlamydomonas (colorized SEM)
- 23. Figure 6.8dc Protistan Cells Flagella 1 µm Nucleus Nucleolus Vacuole Chloroplast Cell wall Chlamydomonas (colorized TEM)
- 24. Cell Biology and Diabetes
- 25. Insulin
- 32. Red arrows indicate Beta Cells
- 63. Figure 11.5a Local signaling Target cell Electrical signal along nerve cell triggers release of neurotransmitter. Neurotransmitter Secreting Secretory diffuses across cell vesicle synapse. Local regulator diffuses through Target cell extracellular fluid. is stimulated. (a) Paracrine signaling (b) Synaptic signaling
- 64. Figure 11.5b Long-distance signaling Endocrine cell Blood vessel Hormone travels in bloodstream. Target cell specifically binds hormone. (c) Endocrine (hormonal) signaling
- 65. Figure 11.6-1 EXTRACELLULAR CYTOPLASM FLUID Plasma membrane 1 Reception Receptor Signaling molecule
- 66. Figure 11.6-2 EXTRACELLULAR CYTOPLASM FLUID Plasma membrane 1 Reception 2 Transduction Receptor Relay molecules in a signal transduction pathway Signaling molecule
- 67. Figure 11.6-3 EXTRACELLULAR CYTOPLASM FLUID Plasma membrane 1 Reception 2 Transduction 3 Response Receptor Activation of cellular response Relay molecules in a signal transduction pathway Signaling molecule
- 70. Figure 11.7c Signaling Ligand-binding site molecule (ligand) α helix in the Signaling membrane molecule Tyr Tyr Tyr Tyr Tyr Tyrosines Tyr Tyr Tyr Tyr Tyr Tyr Tyr Tyr Tyr Tyr Tyr Tyr Tyr CYTOPLASM Receptor tyrosine Dimer kinase proteins 1 (inactive monomers) 2 Activated relay proteins Cellular P Tyr Tyr P Tyr Tyr P Tyr Tyr P response 1 Tyr Tyr P Tyr Tyr P P Tyr Tyr P Tyr Tyr P Tyr Tyr P P Tyr Tyr P Cellular 6 ATP 6 ADP response 2 Activated tyrosine Fully activated kinase regions receptor tyrosine (unphosphorylated kinase Inactive dimer) (phosphorylated relay proteins 3 4 dimer)
- 71. Figure 11.7d 1 2 3 Gate closed Ions Gate Gate closed Signaling open molecule (ligand) Plasma Ligand-gated membrane ion channel receptor Cellular response
- 73. Figure 11.10 Signaling molecule Receptor Activated relay molecule Inactive protein kinase 1 Active protein Ph kinase os 1 ph or Inactive yla protein kinase ATP ADP P 2 tio Active protein n ca PP kinase s Pi 2 ca de Inactive protein kinase ATP 3 ADP P Active protein PP kinase Pi 3 Inactive protein ATP ADP P Active Cellular PP protein response Pi
- 74. Figure 11.10a Activated relay molecule Inactive protein kinase 1 Active protein Ph kinase os 1 ph or Inactive yla protein kinase ATP ADP P tio 2 Active n protein ca PP kinase sc Pi 2 ad e Inactive protein kinase ATP ADP P 3 Active protein PP kinase Pi 3 Inactive protein ATP ADP P Active protein PP Pi
- 75. Fight or Flight
- 77. 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)
- 80. Insulin Receptor - TKR
- 82. Figure 11.12 First messenger (signaling molecule such as epinephrine) Adenylyl G protein cyclase G protein-coupled GTP receptor ATP Second cAMP messenger Protein kinase A Cellular responses
- 83. Figure 11.11 Adenylyl cyclase Phosphodiesterase Pyrophosphate H2O P Pi ATP cAMP AMP
- 84. Figure 11.11a Adenylyl cyclase Pyrophosphate P Pi ATP cAMP
- 85. Figure 11.11b Phosphodiesterase H2O H2 O cAMP AMP
- 86. Figure 11.13 EXTRACELLULAR Plasma FLUID membrane Ca2+ ATP pump Mitochondrion Nucleus CYTOSOL Ca2+ pump Endoplasmic Ca2+ reticulum ATP pump (ER) Key High [Ca2+ ] Low [Ca2+ ]
- 87. Figure 11.14-1 EXTRA- CELLULAR Signaling molecule FLUID (first messenger) G protein DAG GTP G protein-coupled PIP2 Phospholipase C receptor IP3 (second messenger) IP3-gated calcium channel Endoplasmic Ca2+ reticulum (ER) CYTOSOL
- 88. Figure 11.14-2 EXTRA- CELLULAR Signaling molecule FLUID (first messenger) G protein DAG GTP G protein-coupled PIP2 Phospholipase C receptor IP3 (second messenger) IP3-gated calcium channel Endoplasmic Ca2+ reticulum (ER) Ca2+ (second CYTOSOL messenger)
- 89. Figure 11.14-3 EXTRA- CELLULAR Signaling molecule FLUID (first messenger) G protein DAG GTP G protein-coupled PIP2 Phospholipase C receptor IP3 (second messenger) IP3-gated calcium channel Various Cellular Endoplasmic Ca2+ proteins reticulum (ER) responses activated Ca2+ (second CYTOSOL messenger)
- 91. Figure 11.15 Growth factor Reception Receptor Phosphorylation cascade Transduction CYTOPLASM Inactive Active transcription transcription factor factor Response P DNA Gene NUCLEUS mRNA
- 94. Igf-1
- 98. 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 insulin- The full picture. producing b cells (green). Human ES cells can eventually give CREDIT: SEABERG ET AL., NATURE rise to cells that resemble pancreatic BIOTECHNOLOGY beta cells (labeled β).
- 107. Figure 11.2 α factor Receptor 1 Exchange of mating factors a α a factor Yeast cell, Yeast cell, mating type a mating type α 2 Mating a α 3 New a/α cell a/α
- 108. Figure 11.17 RESULTS Wild type (with shmoos) ∆Fus3 ∆formin CONCLUSION 1 Mating Mating Shmoo projection factor factor G protein-coupled forming activates receptor Formin receptor. P Fus3 Actin GTP P subunit GDP 2 G protein binds GTP Phosphory- and becomes activated. lation Formin Formin cascade P 4 Fus3 phos- phorylates formin, Microfilament Fus3 Fus3 activating it. P 5 Formin initiates growth of 3 Phosphorylation cascade microfilaments that form activates Fus3, which moves the shmoo projections. to plasma membrane.
- 111. Cell Membranes and Transport Honors Biology ~ Edgar
- 116. Osmosis
- 121. Osmosis
- 123. 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?
- 125. 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) Add more water to the left hand side. b) Add more water to the right hand side. c) Add more solute to the left hand side. d) Add more solute to the right hand side.
- 126. 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.
- 128. Vegetables in Sucrose Solutions 30.00 Percent Change in Mass (%) 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 1.2 Sucrose Concentration (Molarity)
- 132. Jmol
- 133. Harvard BioVisions
Editor's Notes
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Figure 6.8 Exploring: Eukaryotic Cells
- Blood vessels are the body's plumbing, supplying food and oxygen and removing waste. Now two papers published online this week by Science show that blood vessels play a more active role than previously believed: Even before they start to function, blood vessels help the liver and pancreas develop. In 1995, cancer researchers found the first evidence that there's more to blood vessels than meets the eye. They reported that endothelial cells, which make up blood vessel walls, produce growth factors, indicating they may play some role in development. The new studies build on that work. The first team, led by Douglas Melton of Harvard, began scrutinizing blood vessels after noticing that the endoderm--embryonic tissue fated to become the pancreas and other organs--touches a major blood vessel, the dorsal aorta. Because the developed pancreas monitors blood vessels, measuring glucose levels and producing insulin accordingly, the researchers wondered whether the pancreas and dorsal aorta also communicated during development. To test this, they performed experiments such as growing mouse endoderm in culture with and without embryonic dorsal aortae. Only alongside the blood vessel did the tissue produce pancreas-specific markers, including insulin. The second group, led by Kenneth Zaret of the Fox Chase Cancer Center in Philadelphia, took a different approach. They examined how mouse livers develop when a gene called flk-1 , which encodes a receptor for VEGF, is mutated so that no endothelial cells develop in the liver. When they grew these liver cells in petri dishes, the flk-1 culture grew to the same size as the normal culture but contained far less liver tissue, growing connective tissue instead. Surprisingly, the endothelial cells' influence arose well before the cells fully formed into vessels, suggesting that the cells themselves--and not some component of the blood--are sending the growth signal. Understanding how cells define themselves in an embryo is critical to designing stem-cell-based treatments for disease. "If we're going to induce organs to form, we have to have a thorough understanding of how the embryo develops them," says organ replacement biologist Michael Longaker of Stanford University School of Medicine in Palo Alto, California. "We will never do it in a more elegant way than the embryo."
- Insulin is labelled here in green, glucagon in red, and the nuclei in blue
- 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.
- Figure 11.7 Exploring: Cell-Surface Transmembrane Receptors
- Figure 11.7 Exploring: Cell-Surface Transmembrane Receptors
- 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 11.10 A phosphorylation cascade.
- Figure 11.10 A phosphorylation cascade.
- Figure 11.16 Cytoplasmic response to a signal: the stimulation of glycogen breakdown by epinephrine.
- Figure 11.12 cAMP as a second messenger in a G protein signaling pathway.
- Figure 11.11 Cyclic AMP.
- Figure 11.11 Cyclic AMP.
- Figure 11.11 Cyclic AMP.
- Figure 11.13 The maintenance of calcium ion concentrations in an animal cell.
- Figure 11.14 Calcium and IP 3 in signaling pathways.
- Figure 11.14 Calcium and IP 3 in signaling pathways.
- Figure 11.14 Calcium and IP 3 in signaling pathways.
- Figure 11.15 Nuclear responses to a signal: the activation of a specific gene by a growth factor.
- 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.
- A woman in Japan has had her diabetes reversed by a transplant of insulin-producing cells from her mother. The procedure has given strikingly fast results and marks a departure from previous operations, which relied on cadaver organs as a source of the cells. The first successful transplantation of such cells, called islet cells, from the pancreas of a non-living donor to a diabetic patient was performed in 2000. Since then, about 100 people have had their diabetic condition reversed by the procedure. But waiting for a suitable donor can be a problem, particularly in countries such as Japan, where traditional beliefs against removal of organs from the deceased means that donors are in short supply. For this reason, a team led by Shinichi Matsumoto of Kyoto University Hospital decided to investigate the possibility of extracting islet cells from a live donor. Their first patient was a 27-year-old woman who had become dependent on daily insulin shots after suffering inflammation of the pancreas at a young age. Her 56-year-old mother was the donor. Delicate procedure In a day-long operation, the team transplanted about 10mL of tissue from the pancreas of the mother to the daughter. The procedure was a tricky one, since islet cells are notoriously delicate. "It's difficult to extract them and keep them healthy," explains islet transplantation expert Stephanie Amiel of King's College London, UK. She adds that the cells sometimes form clots after the operation. Matsumoto says that transplants taken from live donors make for healthier cells. Both mother and daughter fared well, he says, and 22 days after the surgery, the young woman no longer needed insulin injections to regulate her blood sugar. "From our experience, this patient has more than double the blood insulin level compared with patients who received one cadaveric islet transplantation," says Matsumoto. The researchers say that people who receive cells from non-living donors tend to become insulin independent only after two or three such procedures. ADVERTISEMENT Amiel says that the daughter's speedy recovery from the recent operation is remarkable given that she only received islets from a portion of the pancreatic tissue; most procedures involve transplanting cells from the entire organ. But Amiel also adds that because the surgery took place in January, the long-term benefits are unclear. "These are quite early days," he says. Matsumoto says he plans to conduct a further 10 such operations this year.
- 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?