gene may play a role in memory - university place … · before the new study, ... said steven...

Blackline Master 2.1 News Articles [Learning Experience 1]

Insights in Biology Blackline Master 2.1page 1 of 9

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Life would be difficult without memories. Andmemories might be difficult without a gene calledNPAS2, Dallas scientists say.

Local researchers have found that without thisgene, mice have trouble learning how to know whensomething scary is about to happen. That’simportant for mice to survive out in the wilderness,or even under the kitchen counter.

And for scientists, the gene’s connection tomemory is an opportunity to study how the braintakes in information and stores it for future use.

“It’s a tantalizing beginning,” said Eric Kandel,a neuroscientist from Columbia University in NewYork. “It whets one’s appetite for more.”

Researchers from the University of TexasSouthwestern Medical Center at Dallas reported thediscovery in the latest issue of the journal Science.

They noted that the gene may also beconnected to the body’s internal clock that keepstrack of day and night.

“There might be rhythmicity in the brain thatmight be important for optimal . . . functioning,said Dr. Joseph Garcia of UT Southwestern.

Before the new study, scientists already knewthat the NPAS2 gene was active only in the brain,where it orchestrates production of a special proteinmolecule. That protein’s job, scientists believe, is toact as a coach, spurring other genes into action.

But to really understand what NPAS2 does inthe brain, the researchers wanted to see how micewould fare when the gene was disabled. So using thetricks of genetic engineering, the UT Southwesternscientists made mice with malfunctioning NPAS2gene. Because the gene was known to work in thebrain, the researchers tested the mice’s mental abilities.

The mice, Dr. Garcia said, went through abattery of tests and did well on all of them, with oneexception. The test required mice to learn that astaticlike noise signaled an impending mild electricalshock to their feet. Mice without the gene had moretrouble on the test. So it seems, Dr. Garcia said, thatthe mice need that gene to remember certainemotional events.

Other scientists said it was hard to know whatto make of the findings.

Dr. Kandel noted that while the mice did worseon one test, they didn’t fail it outright.

“That is not a whopping change,” he said.More research is needed to understand exactly

how the gene helps the brain work.“We don’t have a sense of how it fits into other

molecules that might be important in memory,” Dr. Kandel said.

One way the gene may fit in with other brainmolecules is through a connection with an internalbiological clock, said Steven McKnight, another UTSouthwestern scientist involved in the study.NPAS2 has all the telltale signs of fitting into thenetwork of proteins and genes that help organismskeep track of day and night.

These internal timekeepers, known ascircadian clocks, control body temperature, bloodpressure and other biological processes that changeon a 24-hour cycle. In recent years, scientists havefound many “cogs” and “gears” of these clocks in avariety of organisms.

The protein produced by the NPAS2 gene looksa lot like one of the clock proteins, Dr. McKnightsaid, and more studies are being done to find out howthe gene behaves during the day-night cycle.

Gene May Play a Role in Memoryby Sue Goetinck Ambrose, The Dallas Morning News, June 26, 2000

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For now, the scientists are speculating thatNPAS2 somehow changes nerve cells as day turns tonight and again when night yields to day. Withoutthe NPAS2 gene, that natural cycling may bedisrupted, he said. That may explain why the brainis generally sharper during the day than at night.

“If you don’t have that nice cyclic pattern, andare not getting appropriate rest, then the alert phasewill simply be less alert,” Dr. McKnight said.

Other scientists participating in the researchwere UT Southwestern’s Di Zhang, Sandi Jo Estill,Carolyn Michnoff, Jared Rutter, Martin Reick,Kristin Scott and Ramon Diaz-Arrastia.

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Centuries ago, Big Boys were tiny tots. So were othertasty tomatoes, from Beefsteaks to Celebrities.

Now scientists have found a gene that helpedtransform tomatoes from miniature morsels intoTexas-sized treasures.

The discovery of that gene could help traceback the domestication of wild plants and provideideas for domesticating new plants. Not only that,the tomato gene appears to be similar to a humancancer gene, so it could help researchers understandwhy tumors form. And the discovery should also aidresearchers seeking the genetic roots of common yetcomplicated human diseases like high blood pressure,diabetes and obesity.

“I would say they’ve set an example here for allof us that brings out hope,” said Jim Cheverud, ageneticist at Washington University in St. Louis.“Even though it’s fruit size in tomatoes, it’s the samekind of gene we’re looking for in complex diseases.”

The newly discovered gene has a long history,dating back to wild tomatoes growing in Central andSouth America. The gene helped make the tomatoesnow found on grocery shelves into giants that dwarftruly wild tomatoes.

“If you were out walking around, you probablywouldn’t even notice a wild tomato,” said StevenTanksley, the Cornell University scientist who ledthe tomato gene research. “The wild versions areabout the size of a blueberry.”

Over the years, people domesticated the wildtomatoes, choosing plants that made bigger andbigger fruit. Now the fruits are so large that plantscan’t support them without the help of stakes orcages. The gene responsible for that change isdescribed in the latest issue of the journal Science.

Fruit size is known in the genetics world as aquantitative trait, one that has a wide range withlots of sizes in between. In people, one of the most

obvious of these traits is height. Human heightvaries from under 5 feet to over 7 feet, and there arepeople at every increment in between.

But height is not the only quantitative trait inpeople. Heart disease strikes some people early inlife, others later, and many in between. Bloodpressure, which is partly due to genetics, also has acontinuous range.

Research has shown that the genes behindthese types of traits are plentiful. That’s in sharpcontrast with genetic diseases like cystic fibrosis,where a single gene dictates whether a person hasthe disease. Genes like the one that causes cysticfibrosis are relatively easy to find, said John Doebley,a biologist at the University of Wisconsin-Madison.

“People have cracked that nut,” Dr. Doebleysaid. “But almost all of those diseases affect a smallminority of the population.”

The genes that contribute to conditions likeheart disease are harder to track down, because eachgene on its own has such a small effect.

“There’s where most of the problem is, andthere’s where our knowledge is the weakest,” Dr. Doebley said.

Studies like Dr. Tanksley’s offer hope that thosegenes can actually be found, giving scientists betterammunition in the fight against disease, Dr. Doebleysaid.

Another bonus from the tomato research wasfiguring out exactly how the gene changed to makesmall tomatoes get big. The gene, it turns out, guidesthe production of a protein that acts as a brake oncells. The more the gene works, the less often cellsin the growing fruit divide. That makes for fewercells and smaller fruit.

Over the years, Dr. Tanksley found, the brakinggene changed subtly to work less and less. Indomestic tomatoes, the gene is quiet enough that

Fat-Tomato Gene Yields Disease-Fighting Insightby Sue Goetinck Ambrose, The Dallas Morning News, July 10, 2000

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fruit cells can divide many times more, resulting inbigger fruit.

Similar differences in gene work habits mayexplain why some people are more or less susceptibleto certain diseases.

In the new research, the tomato genehappened to be similar to a gene associated withhuman cancer. Just as the tomato gene governs celldivision in the growing fruit, the human genegoverns the uncontrollable growth of tumor cells.That’s an example of the similarity of all life onEarth, Dr. Tanksley said.

“It could mean that the basic cell . . .mechanisms are very ancient and predate plants andanimals,” he said.

Dr. Tanksley said he is now scrutinizing thegene in all sorts of tomato varieties, both wild anddomestic. So far, he’s found that the largercommercial varieties like Beefsteak and Roma havethe version of the gene that allows for lots of fruitcell division. He and his colleagues are also trackingdown other genes that affect fruit size.

The tomato research may eventually lead tonew ideas for food, Dr. Tanksley said. Rather thanrelying on the plants people have already tamed, itmight be possible to domesticate new species, usingfruit size genes as a guide.

“It’s possible,” he said, “that we’ll have arenewal of domestication.”

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Earwax production is controlled by a gene linked toa very rare movement disorder, UC Irvine andJapanese researchers have found.

The findings, published in the June 8 issue ofLancet, demonstrates how rare disorders can uncovergenetic relationships within the body and may helpresearchers prevent cancer and excessive body odor.

Dr. Hiroaki Tomita, a postdoctoral fellow atUCI’s department of psychiatry, and his colleagues inJapan found from studying the gene for a rare geneticdisorder called paroxysmal kinesigenic choreo-athetosis (PKC) that the gene for producing earwaxwas in the same area as the gene for PKC. Earwaxcomes in two types—the “wet” variety seen mostoften in Caucasians and African-Americans, and the“dry” variety common among Asians and NativeAmericans.

“A woman in our PKC study said that herfamily members who had the disease also had the‘wet’ form of earwax, which is less common inJapan,” Tomita said. “We already knew where thegene for PKC was located, and we found the likelygenes for producing earwax in the same chromosomeregion responsible for producing PKC.”

The researchers, working in Japan, studied 92members of eight families who had at least onemember with PKC and found the gene for earwax onthe 16th chromosome, exactly where the gene forPKC is located. The same team discovered thelocation of the PKC gene in 1999.

While the two genes do not appear to regulateeach other, a gene for PKC happens to be locatedvery closely to the gene for earwax. It is not knownhow the mutations came to lie closely to each otheron the 16th chromosome.

The glands that secrete earwax are calledceruminal glands, which are part of a family oforgans called apocrine glands. Apocrine glands arefound in the armpits and breast. Previous researchhas suggested a relation between wet earwax andhigher rates of breast cancer, which could beconnected by the gene that produces earwax andcontrols apocrine gland function. Apocrine glandsalso produce sweat in the armpit and contribute tobody odor.

“There is not much information about how theapocrine glands are regulated and how they operate,”Tomita said. “We’ve located the position of this geneon the 16th chromosome, but we now need todetermine its exact sequence and starting and endingpoints. If we can pinpoint this, it might give us abetter understanding of how earwax, sweat andapocrine secretions in the breast are controlled.Once pinpointed, characterizing a responsible genefor earwax may contribute to the understanding ofapocrine gland development, body odor and breastcancer.”

Tomita, a postdoctoral fellow at UCI for thepast two years, continues to work with his Japanesecolleagues on finding more information about thegene responsible for PKC, as well as for earwax andother apocrine gland functions.

Tomita came to UCI from the NagasakiUniversity School of Medicine. His colleaguesinclude Dr. Koki Yamada, Dr. Mohsen Ghadami,Takako Ogura, Yoko Yanai, Dr. Yatsumi Nakatomiand Dr. Norio Niihawa of Nagasaki University, Dr. Miyuki Sadamatsu and Dr. Nobumasa Kato ofthe University of Tokyo and Dr. Akira Matsui ofShiga University of Medical Science.

Gene That Produces Earwax Located:Accidental Discovery from Rare DisorderStudy May Help Prevent Breast Cancer,Body OdorUniversity of California, Irvine, June 13, 2002

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Inheriting a variation in a single gene can determinewhether a person will be a wimp or a stoic when itcomes to handling pain.

University of Michigan neuroscientists puthealthy young adults inside a brain scanner, madethem hurt—just temporarily—and proved thatcarriers of the “stoic” gene version really can toleratemore pain.

The discovery emphasizes the need tocustomize pain treatment and might even allowdoctors to soon try predicting which patients willrespond to a certain kind of medication.

People’s perceptions of pain are tremendouslyvariable. A substantial blow to one person may seemtrivial to another; likewise, pain medication thathelps one patient may do nothing for the next.

The new research shows how much peoplesuffer is due partly to a gene that helps regulate howmany natural painkillers, called endorphins, thebody produces.

The gene produces an enzyme called COMTthat metabolizes the neurochemical dopamine,which acts as a signal messenger between brain cells.

Everyone has two copies of this gene, oneinherited from each parent—but they can inheritforms that differ by one amino acid. The COMTgene that contains the amino acid methionine, ormet, is less active than if it contained the amino acidvaline, or val.

Dr. Jon-Kar Zubieta injected the jaw muscles of29 healthy young adults with enough salt water tomake them really ache, simulating a painfulcondition called temporomandibular joint syndrome,or TMJ. Using a PET scanner, Zubieta measured howtheir brain cells reacted while the volunteer victimsrated, every 15 seconds, how much they hurt duringthe 20-minute pain cycle.

People who had two copies of the val-COMTgene were stoics. They withstood significantlygreater saline doses than other volunteers whilerating the resulting pain as less bothersome, Zubietareports in Friday’s edition of the journal Science.

The PET scans verified that response:Painkilling endorphins were much more active inthese people’s brains.

In contrast, people with two copies of the met-COMT gene suffered the most pain from thesmallest saline injections—and had far less naturalpainkiller action.

People who inherited both a met and val genecopy tolerated pain at levels between the twoextremes.

A quarter of the U.S. population carries the“stoic” gene variation while another quarter has thegene variant that makes them supersensitive to pain,Zubieta estimates.

Why would a gene that regulates dopaminealso affect painkilling endorphins? Too muchdopamine in the brain reduces endorphin content,Zubieta explained. People with the double-val genemake a very potent COMT enzyme that clears outdopamine rapidly, triggering more endorphinproduction, while people with the double-met genehave the opposite reaction.

It’s an important discovery, said neurobiologistAdron Harris of the University of Texas at Austin,who has long studied why men and women toleratepain differently.

One reason: When standard pain medicationsfail, antidepressants that target dopamine sometimesrelieve severe, chronic pain. But there has been noway to predict who might benefit. The new researchsuggests a simple gene test might soon solve thatproblem, Harris said.

Gene Helps Determine How Much You HurtLauran Neergaard, The Associated Press, February 21, 2003

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“Certainly the need to individualize paintreatment . . . is great, and is now done mostly bytrial and error,” he said. “This (research) is reallygetting to molecular medicine or genetic medicine,where you’re using the genotype to predict whichdrug would be best for the person.”

Pain response clearly depends on more than asingle gene, Zubieta cautioned. For example, in

another study, he found women tolerate pain betterduring the time of the menstrual cycle whenestrogen levels are highest.

And Zubieta’s ultimate goal isn’t just to predictpain tolerance, but to understand what combinationof genetics and other factors make certain peoplemore vulnerable to painful diseases, like the joint-afflicting fibromyalgia that tends to strike women.

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Treating obesity in humans might be possible bytargeting a gene similar to one that causes growth offat tissue in mice, researchers at the University ofMedicine and Dentistry of New Jersey said Monday.

Mice that do not have or only partially expressa gene called HMGI-C do not gain weight, even ifthey are fed a high-fat diet, according to a studyheaded by Kiran Chada, a biochemist and director ofthe Genomics Center at UMDNJ-Robert WoodJohnson Medical School.

HMGI-C, a gene crucial to cell growth anddifferentiation during development of an embryo,usually is not seen in adult tissues, Chada said. Thegene, however, was found in the fat tissue of micethat became obese on a high-fat diet, and not in leanmice, he said.

Since the HMGI-C gene is 98 percentidentical in mice and humans, people who have thegene and eat fatty foods can expect to become obese,because their undifferentiated cells will grow into fattissue, Chada said.

Now that the gene is known, a drug treatmentcan be developed that inhibits a protein in the genethat triggers other genes that make fat, he said.

The results of Chada’s study were publishedMonday in the journal Nature Genetics. Theresearch was funded by the National Institutes ofHealth and the New Jersey Commission on Scienceand Technology.

“This gene is one of the most exciting potentialtargets [of obesity] that we have,” Chada said in aninterview. One thing that makes the gene soimportant is that it affects a very specific area, headded.

“When we see mice with a high-fat dietsuddenly put on weight, this gene is expressed onlyin fat tissue. All the other organs and tissues of micedo not express the gene,” he said.

This means that a drug can be developed totreat just the gene in fat cells, with limited sideeffects on other tissues, Chada said.

What also excited Chada was that not onlymice without the gene did not gain weight. Micewith partial expression—having one copy ratherthan two copies—of the HMGI-C gene also stayedslim on a fatty diet.

So a drug treatment for obesity would onlyhave to reduce the gene’s activity by 50 percent—instead of the usual 100 percent—to effectively stopproduction of fat cells, he said.

Three New Jersey pharmaceutical companieshave expressed interest in developing an obesity drugbased on Chada’s work, which is patented by RutgersUniversity, he said. A drug could be developedwithin 11⁄2 years, with another five to 10 years forclinical trials, Chada said.

The drug, which would inhibit the gene, wouldbe different from diet drugs that work on the nervoussystem, often with side effects, to make people eatless and modify their behavior, he said. It also doesnot affect how fats are absorbed by the body. Aperson using this drug would simply eliminate extrafat instead of storing it, he said.

“Our approach is different. We’re saying, ‘Let’sforget about changing people’s behavior by messingwith the central nervous system. Let’s attack thetissue where fat is made. Eat as much as you like,then, because you’re taking the drug that will notallow you to make fat cells,” Chada said.

“Unfortunately, even with the best geneinhibitor, there’s no guarantee it’ll work. There couldbe 101 other factors” causing obesity, he said.

Behavioral scientists acknowledge that genesplay a big role in obesity, but other factors alsocontribute to the condition, said Terence Wilson, apsychologist at Rutgers in Piscataway.

Mouse Gene May Help Fight ObesityReproduced with permission of The Record (Bergen County, NJ). Bob Groves, March 28, 2000.

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“There is very good evidence of geneticpredisposition to obesity. But whatever those genesare, they have to be expressed in a particularenvironment,” said Wilson, director of the EatingDisorders Clinic at Rutgers.

The affluence, sedentary lifestyle, andubiquitous junk food of American culture create a“toxic environment responsible for alarming rates ofobesity in this country,” he said. Psychologicalfactors are also involved. Some people rely on foodto deal with emotions, he said.

People would like a “quick fix” for obesity withgene therapy, but the disorder involves a “complex

set of events. Even if we identify the genes, we’restill not going to be able to disregard environmental,cultural, and individual factors,” Wilson said.

Treating and preventing the life-threateningeffects of obesity, such as diabetes and heart disease,are as crucial as finding the cause of the disorder, hesaid.

“I and any other behavioral scientist wouldwelcome a breakthrough in biological research” ofobesity, Wilson said. “There have been other genesidentified for obesity. It’s a thriving area of research,and important discoveries are being made.”

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Blackline Master 2.2 Pedigree: Blue People of Kentucky [Learning Experience 3]


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1I

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8obligate carrierprobable carrier

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Pedigree Pedigree Position Name Position Name

I-1 Benjamin Fugate (bd ca. 1750) II-1 Martin Fugate (bd ca. 1783)

I-2 Hannah ?? (bd 1783) II-2 Mary ?? (Ritchie?/Smith?) bd 1780)

I-3 William Smith II-3 Richard Smith (bd 1771)

I-4 ?? Betty Ritchie (bd ca. 1750)/Eunice ?? II-4 Alicia Combs (bd 1775/80)

I-5 Nicholas Combs (bd before 1764) II-5 Levi Fugate (bd 1795)

I-6 Nancy Gribsby (bd ca. 1750) II-6 Haney Noble (bd 1790)

I-7 William Fugate (bd 1760/65)

I-8 Jane ??

III-1 Hannah Fugate (bd 1811/12 IV-1 Martin Ritchie (bd 1829)

III-2 James Ritchie (bd ca. 1806) IV-2 Rebecca Williams (bd )

III-3 Andrew Fugate (bd 1808) IV-3 William Fugate (bd 1838)

III-4 ??? IV-4 Juda Campbell (bd 1837)

III-5 Zachariah “Ball Creek Zach” Fugate IV-5 John “Blue” Fugate (bd 1832)(bd 1817)

III-6 Mary Smith (bd 1814) IV-6 Zachariah Fugate (bd 1845)

III-7 Martha Smith (bd 1798) IV-7 Polly Campbell (bd 1844)

III-8 John Campbell (bd 1796) IV-8 Lettie M. Smith (bd 1834)

III-9 Sara “Sally” Fugate (bd ) IV-9 Elizabeth Campbell (bd 1827)

III-10 Lorenzo Dow Smith (bd 1816) IV-10 Henry Hudson (bd 1827)

III-11 Elizabeth Smith (bd 1816)

III-12 Martin Fugate (bd 1856)

V-1 James “Big Jim” Ritchie (bd 1857) VI-1 Gabriel Fugate (bd 1890)

V-2 Hannah Fugate (bd 1856) VI-2 Zachariah “Big Man” Fugate (bd1884)

V-3 Eleanor Fugate (bd 1860) VI-3 Elizabeth “Aunt Bessie” Fugate (bd 1876)

V-4 Lorenzo “Blue Anze” Fugate (bd 1854) VII-1 Mahala Ritchie (bd 1854)

V-5 Polly “Poss” Ritchie (bd 1886) VII-2 Levi Fugate (bd 1844)

V-6 Manuel “Man” Fugate (bd 1879)

V-7 Nancy Hudson (bd 1849/50) VIII-6 Luna Fugate (bd 1889)

V-8 Charles Fugate (bd 1846) VIII-7 John C. Stacey

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Blackline Master 2.3 DNA Model Pieces [Learning Experience 4]


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S

S

adenine

adenineAttach sugar moleculeto lower corner.

Attach sugar moleculeto lower corner.

hydrogen bonds

hydrogen bonds

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r thymine

thymineS

S

hydrogen bonds

hydrogen bonds



S

S

guanine

guanineAttach sugar moleculeto lower corner.


hydrogen bonds

hydrogen bonds

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r cytosine

cytosineS

S

hydrogen bonds

hydrogen bonds



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to base

left

sugar

to base

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sugar

to base

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sugar

to base

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sugar

to base

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sugar

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sugar

to base

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sugar

to base

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sugar

to base

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sugar

to base

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sugar

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phosphate

phosphate

left

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phosphate

phosphate

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phosphate

phosphate

left

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phosphate

phosphate

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phosphate

phosphate

left

right

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Blackline Master 2.4 Alternative Codon Table [Learning Experience 5]


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G

G

G

A

A

A

C

C

CU

UU

GACU

GACU

GACU

UUUUUCUUAUUG

CUUCUCCUACUG

AUUAUCAUAAUG

GUUGUCGUAGUG

UCUUCCUCAUCG

CCUCCCCCACCG

ACUACCACAACG

GCUGCCGCAGCG

UAUUACUAAUAG

CAUCACCAACAG

AAUAACAAAAAG

GAUGACGAAGAG

UGUUGCUGAUGG

CGUCGCCGACGG

AGUAGCAGAAGG

GGUGGCGGAGGG

phe

leu

leu

ile

met

val

ser

ser

pro

thr

ala

tyr

stopstop

stop

his

gln

asn

lys

asp

glu

arg

arg

gly

cys

trp

First

lette

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end)

Second letter

Third letter (3' end)

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Blackline Master 2.5 The mRNA Sequences of Normal and Sickling Hemoglobin [Learning Experience 6]These are segments of the mRNA codons for a normal, β-globin gene and for a sickle-cell, β-globingene. Use the genetic code table (Table 2.3) in your Student Edition to find the corresponding aminoacid sequence for each gene.

NORMAL OR HEMOGLOBIN A (mRNA):

AUGGUGCACCUGACUCCUGAGGAGAAGUCU...

SICKLING OR HEMOGLOBIN S (mRNA):

AUGGUGCACCUGACUCCUGUGGAGAAGUCU...


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Blackline Master 2.6 Human Karyotype [Learning Experience 7]


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Blackline Master 2.7 Chromosome Smears 1–9 [Learning Experience 7]

Chromosome Smear 1


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Chromosome Smear 2


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Chromosome Smear 3


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Chromosome Smear 4


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Chromosome Smear 5


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Chromosome Smear 6


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Chromosome Smear 7


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Chromosome Smear 8


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Chromosome Smear 9


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Blackline Master 2.8 Karyotype Placement Grid [Learning Experience 7] Chromosome Smear #

Name(s) Date

1 2 3 4 5

6 7 8 9 10 11 12

13 14 15 16 17 18

19 20 21 22 X Y


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Blackline Master 2.9 Information on Chromosome Disorders [Learning Experience 7]

A. Cri-du-chat

This disorder is the result of a deletion in the upper arm of one chromosome number 5. Babies have acry that sounds like that of a cat in distress (hence the name, which means “cry of the cat”). This is theresult of an improperly developed larynx. Cri-du-chat babies are severely mentally retarded and have asmall cranium. The incidence of this syndrome is 1 in 100,000 live births.

Karyotype: 46 XX or 46 XY with a deletion in chromosome number 5

B. Down’s syndrome

This syndrome is the result of an extra chromosome number 21. The disorder results in individuals whoare short in stature and have broad hands, stubby fingers and toes, a wide rounded face, a largeprotruding tongue that makes speech difficult, and mental retardation to varying degrees. Theseindividuals are prone to respiratory infections, heart defects, and leukemia. The risk of having a babywith Down’s syndrome increases with the age of the mother. It ranges from 1 in every 1,500 live birthsfor mothers in their early 20s, to 1 in every 70 for mothers over 35, to 1 in every 25 for mothers 45 or older.

Karyotype: 47 XY or 47 XX with three of chromosome number 21

C. Philadelphia translocation

This disorder is the result of part of one chromosome number 9 being inserted or translocated intochromosome number 22. Individuals with this disorder suffer from chronic myelogenous leukemia. Thisis believed to be the result of two genes normally not on the same chromosome being expressed on thesame chromosome and producing an unusual protein that causes the disease.

Karyotype: 46 XX or 46 XY with a chromosome number 9 translocation to chromosome number 22

D. Turner’s syndrome

This condition is the result of the lack of a second sex chromosome. The resulting individual has one Xand no second X or Y chromosome. These girls tend to be short and have a stocky build, but theyappear to be normal before puberty. At puberty, no secondary sexual characteristics develop. Theyproduce no eggs, and menstruation and breast development do not occur. The frequency is 1 in 2,500live female births.

Karyotype: 45 X with one X chromosome

E. Klinefelter’s syndrome

This disorder is the result of having two X chromosomes and one Y chromosome. Individuals with thissyndrome appear to be normal males, but they have characteristics that include tall stature, smalltesticles, and sterility. This condition occurs once in every 1,000 live male births.

Karyotype: 47 XXY


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Adapted from “Karyotype Succuss Rate Increases with Stylized Chromosomes,” by Caroline Purser, The American BiologyTeacher, September 1987

3507-BLM2.2-2.6.pdf 7/25/06 4:51 PM Page 21

F. Jacobs

This condition is the result of an extra Y chromosome. Men with the condition are tall and have lowmental ability. This condition occurs at a rate of 1 in every 1,000 live male births.

Karyotype: 47 XYY

G. Triple X

Individuals with this condition have three X chromosomes. However, no specific physical or mentalabnormalities are associated with an extra X chromosome. Women who have this condition are normaland fertile.

Karyotype: 47 XXX

H. Edwards syndrome

This syndrome is the result of having an extra chromosome number 18. Symptoms of this conditioninclude severe retardation and physical malformations such as an elongated skull, a very narrow pelvis,low-set ears, and very small mouth and teeth. Nearly all babies born with this condition die in earlyinfancy. The frequency of occurrence is 1 in every 5,000 live births.

Karyotype: 47 XX or 47 XY with three of chromosome number 18

I. Patau syndrome

This condition is the result of an extra chromosome number 13. This results in severely abnormalcerebral functions and almost always leads to death in early infancy. A baby with this syndrome has avery pronounced cleft lip and palate, a small cranium, and nonfunctional eyes, as well as heart defectsand mental retardation. The frequency of occurrence is 1 in every 15,000 live births.

Karyotype: 47 XX or 47 XY with three of chromosome number 13


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Blackline Master 2.10 Concept Map Terms [Learning Experience 8]

Include the following words in your concept map. Remember, there should be verbs (action words) oneach connecting line.

meiosis gametes

chromatid(s) haploid

chromosome diploid

egg oogenesis

sperm spermatogenesis

testis variation

ovary independent assortment

✂

Concept Map TermsInclude the following words in your concept map. Remember, there should be verbs (action words) oneach connecting line.

meiosis gametes

chromatid(s) haploid

chromosome diploid

egg oogenesis

sperm spermatogenesis

testis variation

ovary independent assortment


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Blackline Master 2.11 Crossover [Learning Experience 10]


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B

B B

B

B B

B

B

R

R

RR

R R

R R

R

b

b b

b

b b

b

b

r

r

rr

r r

r r

r

sister chromatids segregating to form gametes

crossover, resulting in homologouschromosomes with a new arrangement

of alleles

crossover occurring between chromatidsin homologous chromosome

chromosome replication, resulting in twosister chromatids in each chromosome

homologous chromosomes

3507-BLM2.2-2.6.pdf 7/25/06 4:51 PM Page 24

Blackline Master 2.12 Queen Victoria’s Descendants [Learning Experience 11, For Further Study]


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Eite

l18

83-1

942

Adalb

ert

1884

-194

8Au

gustu

s18

87-1

949

Crow

n Pr

ince

Fred

erick

Willi

am18

82-1

951

Cecil

ie18

86-1

954

Hube

rtus

1909

-50

Fred

erick

1911

-66

Alex

andr

ine19

15-8

0W

illiam

1906

-40

Doro

thea

1907

-72

Felic

ita19

34-?

Chris

ta19

36-?

Louis

1907

-?M

agda

lene

1920

-?

Anas

tasia

1944

-?

Mar

ie-Ch

ristin

e19

47-?

5

Cecil

ie19

17-7

5

Adelh

eid18

91-1

971

Willa

m19

19-?

Kirb

yun

know

n

Bere

ngar

1948

-?M

arina

1948

-?

Victo

ria19

17-?

Mar

ieun

know

n

Adalb

ert-

Adelh

art

1948

-?

Mar

ie-Lo

uise

1945

-?

1

3507-BLM2.2-2.6.pdf 7/25/06 4:51 PM Page 25

Empe

ror W

illiam

IIof

Ger

man

y18

59-1

941

(reno

unce

d th

e th

rone

191

8)

Char

lotte

1860

-191

9He

nry

1862

-192

9

Augu

sta o

f Sc

hlesw

ig-Ho

lstein

1858

-192

1

Augu

stus

1887

-194

9Os

car

1888

-195

8

Victo

ria

Louis

e of

Prus

sia18

92-1

980

Adelh

eid18

91-1

971

Mar

ieun

know

n

Adalb

ert-

Adelh

art

1948

-?

1

Ina

Mar

ia18

88-1

973

Willa

m19

22-?

Burc

hard

1917

-?In

a M

arie

1917

-?Ch

arles

unkn

own

Char

les19

44-?

Victo

ria19

39-?

Erne

st19

40-?

Mar

ie18

98-1

983

Joac

him18

90-1

920 Ch

arles

1916

-?

Fran

cisW

illiam

1943

-?

Fran

cisJo

seph

1943

Fran

cisFr

eder

ick19

44-?

Erne

st18

87-1

953

Erne

st19

14-8

7Or

trud

1925

-198

0

Ludw

ig19

55-8

9M

arie

1952

-?Er

nest

1954

-?

Osca

r19

15-3

9

Chan

tal

unkn

own

Chris

tian

1985

-?Er

nest

1983

-?1

Olga

1958

-?Al

exan

dra

1959

-?He

inrich

1961

-?

Geor

ge19

15-?

King

Geo

rge

IIof

Gre

ece

1892

-197

2(d

epos

ed 1

923-

35)

Unkn

own


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Quee

nEl

izabe

th II

1926

-?

Albe

rt18

19-6

1

Quee

n Vi

ctoria

of E

nglan

d18

19-1

901

Victo

ria18

40-1

901

Empe

ror

Fred

erick

III

of G

erm

any

1831

-88

Sigis

mund

1864

-66

Henr

y18

62-1

929

Victo

ria18

66-1

929

Wald

emar

1868

-79

Mar

gare

te o

fHe

sse

1870

-193

2

Albe

rt18

64-9

2

King

Geor

ge V

Iof

Eng

land

1895

-195

2

King

Edwa

rd V

IIIof

Eng

land

1892

-197

2(a

bdica

ted)

Princ

eCh

arles

1948

-?

Princ

ess

Dian

a19

61-?

Princ

eW

illiam

1982

-?

Princ

eHe

nry

1984

-?

Princ

ess

Anne

1950

-?

Princ

eAn

drew

1960

-?

Mar

k19

48-?

Sara

hFe

rgus

on19

59-?

Beat

rice

1988

-?Eu

genie

1990

-?Pe

ter

1977

-?Za

ra19

81-?

Mon

ika19

29-?

Alex

andr

a19

59-?

Heinr

ich19

61-?

Irene

1942

-?So

phia

1938

-?Fred

erica

1917

-?

King

Cons

tant

ine II

of G

reec

e19

40-?

(dep

osed

197

3)

Chris

tian

1919

-81

Guelp

h19

23-?

King

Con

stant

ine I

of G

reec

e18

68-1

923

(dep

osed

191

7-20

,ab

dicat

ed 1

922)

King

Geo

rge

IIof

Gre

ece

1892

-197

2(d

epos

ed 1

923-

35)

King

Alex

ande

r Iof

Gre

ece

1893

-192

0(re

ined

1917

-20)

Irene

1904

-?Ay

mon

?-19

48

Amad

eo19

43-?

Rich

ard

unkn

own

Rich

ard

1948

-?

Cath

erine

1904

-?He

len18

96-1

982

King

Pau

l Iof

Gre

ece

1901

-196

4

Soph

ie of

Prus

sia18

70-1

932


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Quee

nEl

izabe

th II

1926

-?

Albe

rt18

19-6

1

Quee

n Vi

ctoria

of E

nglan

d18

19-1

901

King

Edw

ard

VII

1841

-191

0

Alex

andr

a of

De

nmar

k18

44-1

925

Mar

gare

te o

fHe

sse

1870

-193

2

King

Ge

orge

Vof

Eng

land

1883

-194

2

Louis

e18

67-1

931

Albe

rt18

64-9

2M

ary o

f Tec

k18

67-1

953

King

Geor

ge V

Iof

Eng

land

1895

-195

2

Henr

y19

00-7

4M

ary

1897

-196

5M

aud

1893

-194

5Al

exan

dra

1891

-195

9Ge

orge

1902

-42

John

1905

-19

King

Edwa

rd V

IIIof

Eng

land

1892

-197

2(a

bdica

ted)

Eliza

beth

(the

Quee

n M

othe

r)19

00-? Pr

inces

sM

arga

ret

1930

-?

Anth

ony

1930

-?

Princ

eAn

drew

1960

-?

Princ

eEd

ward

1964

-?

Mar

k19

48-?

Sara

hFe

rgus

on19

59-?

Beat

rice

1988

-?Eu

genie

1990

-?Za

ra19

81-?

David

1961

-?Sa

rah

1964

-?

Ragn

hild

1930

-?

Haak

onun

know

nIn

gebo

rgun

know

n

Alex

ande

r18

49-1

912

Arth

ur18

83-1

938

Char

les18

93-?

Alist

air19

14-4

3

David

1961

-?Al

exan

dra

1959

-?

Jam

es19

29-?

Caro

line

unkn

own

Visto

ria18

68-1

935

Mau

d18

68-1

935

Mar

tha

1901

-54


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Alice

1843

-187

8Lo

uis IV

of H

esse

1837

-92

Eliza

beth

1864

-191

8 Geor

ge18

92-1

938

Louis

1900

-79

Victo

ria18

63-1

950

Louis

1854

-192

1

Andr

ew o

fGr

eece

1882

-194

4

Cecil

ie19

11-3

7

John

1871

Louis

1931

-7

Alice

of

Batte

nber

g18

85-1

965

Mar

garit

a19

05-8

1Th

eodo

ra19

06-6

0Ge

orge

1906

-37

Alex

ande

r19

33-7

Joan

na19

36-9

Serg

e18

57-1

905

King

Har

ald V

of N

orwa

y19

37-?

Ragn

hild

1930

-?

Ragn

hild

unkn

own

Haak

onun

know

nIn

gebo

rgun

know

nCh

ristin

a19

33-?

Doro

thea

1934

-?Ch

arles

1937

-?

Louis

e18

89-1

965

Char

les18

93-?

David

1961

-?

Caro

line

unkn

own

Mau

d18

68-1

935

Mar

tha

1901

-54

King

Cha

rles

Haak

on o

f No

rway

1872

-195

7

King

Olav

Vof

Nor

way

1903

-91

Erlin

gun

know

nAs

trid

1932

-?

Haak

on19

73-?

Mat

tha

1971

-?

Sonja

1937

-?

Wald

emar

1889

-194

5


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Alfre

d, D

uke

ofEd

inbur

gh18

44-1

900

Erm

est

1868

-193

7

King

Fer

dinan

d I

of R

oman

ia18

67-1

927

Mar

ie19

00-6

1 Tom

islav

1928

-?

Alice

1843

-187

8Lo

uis IV

of H

esse

1837

-92

Eliza

beth

1864

-191

8 Geor

ge18

92-1

938

Louis

1900

-79

Princ

e Ph

illip

1921

-?

Soph

ia19

14-?

Serg

e18

57-1

905

Fred

erick

1870

-3

Tsar

itsa

Alex

andr

a18

72-1

918

Mar

y18

74-8

Tsar

Nich

olas

1868

-191

8

Olga

1895

-191

8Ta

tiana

1897

-191

8M

arie

1899

-191

8An

asta

sia19

01-1

8

Alex

ei19

04-1

8

Mar

ie, Q

ueen

of R

oman

ia18

75-1

938

Alfre

d18

74-9

9

Eliza

beth

1894

-195

6

King

Mich

ael I

of R

oman

ia19

21-?

(dep

osed

194

7)

Joan

na18

93-1

953

King

Car

ol II

of R

oman

ia18

93-1

953

(dep

osed

194

0)

Son

date

sun

know

n

King

Pet

er II

of Y

ugos

lavia

1923

-70

(dep

osed

194

5)

Irene

1866

-195

3

Chris

tina

1933

-?

Chris

toph

er19

01-4

3(k

illed

in W

WII)

Doro

thea

1934

-?Cl

ariss

a19

44-?

Char

les19

37-?

Raine

r19

39-?

Guelp

h19

47-8

1Fr

eder

icka

1954

-?Ge

orge

1949

-?

Wald

emar

1889

-194

5He

nry

1900

-4Si

gismu

nd18

96-?


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Alfre

d, D

uke

ofEd

inbur

gh18

44-1

900

Mar

ie of

Ru

ssia

1853

-192

0

Nich

olas

1903

-78

King

Fer

dinan

d I

of R

oman

ia18

67-1

927

Victo

ria18

76-1

936

Kirill

1876

-193

8

Mar

ia19

07-5

1Ki

ra19

09-6

7Vl

adim

ir19

17-?

Princ

ess

Mar

gare

tha

1934

-?

Princ

ess

Birg

itta19

37-?

Princ

ess

Desir

ee19

38-?

Mar

ie19

00-6

1 Tom

islav

1928

-?An

drej

1929

-?

King

Alex

ande

r Iof

Yug

oslav

ia18

88-1

934

(ass

assin

ated

)

Mar

ie, Q

ueen

of R

oman

ia18

75-1

938 El

izabe

th18

94-1

956

King

Mich

ael I

of R

oman

ia19

21-?

(dep

osed

194

7)

King

Pet

er II

of Y

ugos

lavia

1923

-70

(dep

osed

194

5)

Ilean

a19

09-?

6

Mirc

ea19

13-6

Alex

andr

a18

78-1

942

4

Daug

hter

1879

Beat

rice

1884

-196

6

3El

izabe

th18

95-1

903

61

Chris

tian

1867

-190

0

7


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Mar

gare

tof

Swe

den

1882

-192

0

Princ

ess

Mar

gare

tha

1934

-?

King

Car

l XVI

of S

wede

n19

46-?

Princ

ess

Birg

itta19

37-?

Princ

ess

Desir

ee19

38-?

Princ

ess

Chris

tina

1943

-?

4

Daug

hter

1879

Beat

rice

1884

-196

6

3

Helen

a18

46-1

923

Chris

tian

1831

-191

7

Chris

tian

1867

-190

0Al

bert

1869

-193

1He

lena

1870

-194

8M

arie

1872

-195

6Fr

eder

ick18

76Ar

ibert

1864

-193

3

Louis

e18

48-1

939

John

1845

-191

4Ar

thur

1850

-194

2

Louis

eM

arga

ret o

fPr

ussia

1860

-191

7

King

Gus

tav V

Iof

Swe

den

1882

-197

3

Princ

e Gu

stav

Adolf

of

Swed

en19

06-4

7

Bern

adot

te19

07-?

Ingr

id19

10-?

Berti

l19

12-?

Bern

adot

te19

16-?

Lilian

1915

-?

King

Fred

erick

IXof

Den

mar

k18

99-1

972

Quee

nM

ergr

ethe

IIof

Den

mar

k19

40-?

Henr

i19

34-?

Fred

erick

1968

-?Jo

achim

1969

-?

Bene

dikt-A

strid

1944

-?Ri

char

d19

34-?

Anne

-Mar

ie19

44-?

Alex

ia19

65-?

Paul

1967

-?Th

eodo

raun

know

nNi

chola

s19

69-?

1Mon

ica19

48-?

Alex

andr

a18

91-1

959

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gene may play a role in memory - university place … · before the new study, ... said steven...

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