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4 Feb 2019

Is it right to assume that the first living organisms on earthhad a linear genome? I base this on the fact that linearmacromolecules are clearly much more common innature that circular ones. To be honest, I can't even think ofany naturally-occurring circular macromolecules that aren't alreadya part of current living organisms.

Were the very first living organisms more likely to havelinear genomes? If so, when during evolutionary time did circularchromosomes originate?

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Reid Wolff
Reid WolffLv2
6 Feb 2019

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What exactly was Hooker's response to Darwin's, Origin of Species? Thank you for your help. I need help deciphering what his opinions truly were.

Hooker, J. D. 1859. [Review of] On the origin of species. Gardeners' Chronicle (31 December): 1052. Part 1.

From the above expressions it will be inferred that we have risen from the perusal of Mr. DARWIN'S book much impressed with its importance, and have moreover found it to be so dependent on the phenomena of horticultural operations, for its facts and results, and so full of experiments that may be repeated and discussed by intelligent gardeners, and of ideas that may sooner fructify in their minds than in those of any other class of naturalists, that we shall be doing them (and we hope also science) a service by dwelling in some detail upon its contents. Thus much we may premise, that it is a book teeming with deep thoughts on numberless simple and complex phenomena of life; that its premises in almost all cases appear to be correct; that its reasoning is apparently close and sound, its style clear, and we need hardly add its subject and manner equally attractive and agreeable; it is also a perfectly ingenuous book, bold in expressions as in thought where the author adduces what he considers clear evidence in his favour, frank in the statement of objections to the hypotheses or conclusions founded on its facts and reasonings; and uniformly courteous to antagonistic doctrines. In fine, whatever may be thought of Mr. DARWIN'S ultimate conclusions, it cannot be denied that it would be difficult in the whole range of the literature of science to find a book so exclusively devoted to the development of theoretical inquiries, which at the same time is throughout so full of conscientious care, so fair in argument, and so considerate in tone. . . . Hitherto most [naturalists] have, as we have already observed, contented themselves with the hypothesis that they were independently created, and the minority have clung to the only other explanation hitherto conceived, that they have all been created by variation from a single first-created living organism, or a few such. Now it must be borne in mind that both these views are mere hypotheses in a scientific point of view; neither has any inherent or prescriptive right to a preference in the mind of the impartial inquirer; but the most superficial observation will show that the hypothesis of original creations is incapable of absolute proof, except the operation be witnessed by credible naturalists, and can only be supported by facts that are either not conclusive against the opposite doctrine, or may be regarded as equally favourable to it; and this hypothesis is hence placed at a disadvantage in comparison with that of the creation of species by variation, which takes its stand on the familiar fact that species do depart from the likeness of their progenitors, both in a wild and domestic state. On the other hand the hypothesis of creation by variation labours under the disadvantage of being founded upon a series of phenomena, the action of each of which individually, as explained by Mr. DARWIN, would appear to prevent the possibility of species retaining their characters for any length of time, and it therefore appears at first sight opposed to the undisputed fact, that many hundreds of animals and plants have transmitted their characters unchanged (or nearly so) through countless generations, and covered, even within the historic period, many square miles of country each with millions of its exact counterpart. To explain this anomaly and to raise this hypothesis of creations by variation to the rank of a scientific theory, is the object of Mr. DARWIN'S book, and to do this he has endeavoured to invent and prove such an intelligible rationale of the operation of variation, as will account for many species having been developed from a few in strict adaptation to existing conditions, and to show good cause how these apparently fleeting changelings may by the operation of natural laws be so far fixed as to reconcile both the naturalist and the common observer to the idea, that what in all his experience are immutable forms of life may have once worn another guise. The hypothesis itself is a very old one; it was, as all the world knows, strongly advocated by LAMARCK, and later still by the author of the "Vestiges of the Natural History of the Creation," but neither of these authors were able to suggest even a plausible method according to which Nature might have proceeded in producing suitable varieties, getting rid of intermediate forms, and giving a temporary stability to such as are recognised as species by all observers. Mr. DARWIN has been more successful, though whether completely so or not the future alone can show. We shall proceed to examine his method in another article.

Roger Maxwell is very health-conscious. He runs, swims, and hikes; follows a lowcarbohydrate diet; and generally feels great. He sees a physician when he needs to, in addition to annual physical exams at the large company where he is an engineer. He'd never allow himself to get so out of shape that heart disease would be a risk. Because of his strict adherence to this healthy lifestyle, Roger is surprised when a medical intern, gazing at his yearly elecfrocardiogram (ECG) at his work physical, clearly picks up on something.

"What? What are you looking at?" Roger blurts out while buttoning up his shirt.

"Oh, it's probably nothing." But she doesn't look like it's probably nothing.

"The heart murmur? My mom's been telling me about it since childhood. Not a big deal. The doctors called it something last year, something I never heard of." "Did you check it out?" asks the intern.

"Nah. It wasn't bothering me, so I forgot about it. Why? What's wrong?"

"Well, maybe you should ask the doctor to explain it again and suggest what to do."

"About what?"

"The doctor will explain it. Please don't worry, though," says the intern as she rushes off to the next patient.

Roger's electrocardiograms had in fact been showing that he has had long QT syndrome, and not a heart murmur, for many years. The doctor explains that this is a problem with the heart's rhythm, and not its valves. Roger goes home and Googles long QT syndrome right away. What he finds concerns him enough to alert his relatives.

Long QT syndrome is a lengthening in the time that it takes the ventricles (the lower two heart chambers) to recover after a contraction, called the QT interval on an electrocardiogram. This delay is called torsade de pointes, and it causes lightheadedness upon standing or even fainting, as blood pressure drops when the heart rhythm becomes abnormal. If the arrhythmia turns into the more erratic condition called ventricular fibrillation, it can be deadly. Some cases •of sudden cardiac arrest in people who apparently do not have heart disease are in fact due to long QT syndrome. This 'may have been the case with Roger's aunt, Amelia, his mother's sister, who died at age 34 of what was thought to be a heart attack, but, now Roger realizes, was more likely an arrhythmia. Still, with only one affected relative, Roger had never thought of his aunt's •early demise as a family history, especially since his mother is healthy.

Roger reads that in people with some forms of long QT syndrome, fatal arrhythmia can be triggered by intense emotions or a sudden loud sound. The first recorded case of the condition was a little girl, who collapsed dead •when her teacher suddenly yelled at her. Her older brother had died in a similar circumstance. Suddenly, Roger remembers that his daughter Sheila faints very easily. She even passed out once at a rock concert because she got so excited. He'd never panicked over it because his mother fainted easily, too. A pattern was emerging.

Long QT syndrome is caused by mutations in any of at least 10 genes that encode either proteins that form parts of ion channels (potassium, sodium, or calcium) or proteins that affect the functioning of these channels. Ion channels control the spread of nerve impulses and the resulting muscle contraction. The time for the heart's reeovery after a beat, called repolarization, extends the period when ions are trapped inside heart muscle cells because the channels are blocked, too slow to open, or too quick to close in people who are at elevated risk due to inheriting a mutation. People with long QT syndrome can experience arrhythmia if they take certain drugs that prolong the QT interval. These drugs include certain antibiotics, antidepressants, and diuretics ("water pills").

Roger reads about the different genes and drug combinations that cause long QT syndrome on Wikipedia, and then he scans www.genetests.org to find labs that test for all of them. Only then does he make an appointment with a cardiologist, and he arranges to have his blood and that of his daughter and mother sent to one of the labs. Two weeks later, he learns that they all have a dominant mutation in a gene called HERG (for "human ether-a-go-go") that causes long QT syndrome type 2 (LQT2). Even healthy family members could have inherited the mutation, because 15 percent of people with long QT syndrome do not have symptoms. The concern is their increased risk of developing symptoms in the future—perhaps suddenly.

Question 1 : Roger is upset that in the past doctors had not been more insistent that he follow up on the abnormal ECG pattern. When he mentions this to his primary care physician, she answers, "I didn't say anything because you are so healthy, and people who have cardiac arrest from long QT do so in young adulthood. You're too old to worry about it." But Roger should be worried, because

a. he looks younger than he is, so could still be at risk

b. the condition can be inherited, so others in the family could be affected.

c. he could die at any time.

d. he can no longer take antibiotics.

e. long QT syndrome can cause cholesterol to build up in his coronary arteries.

2. Individuals who should take genetic tests for long QT syndrome are

a. all the people in generation IV.

b. Eric, Joan and Peter, and then Dylan, Anika, Sean, Keri, and Anna if a parent has the mutation.

c. Juanita, Larry, Joan, Peter, and Ellie.

d. Abe, Sara, Craig, Philip, Edwin, and Yvonne.

e. Only those who are athletic.

3. The mode of inheritance of long QT syndrome in the Maxwell family is

a. X-Iinked recessive

.b. autosomal recessive.

c. autosomal dominant.

d. sex-limited.

e. X-Iinked dominant.

4. Some people who inherit the same mutation as Roger do not experience any symptoms. This means that the mutation is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e. dominant.

5). The fact that mutations in any of several genes can cause long QT syndrome means that the condition is

a. variably expressive.

b. genetically heterogeneic.

c. polygenic.

d. incompletely penetrant.

e.recessive.

6). The risk that Sean, Keri, or Anna has inherited the family's mutation for long QT syndrome is

a. 1

b. ¾

c. ¼

d. ¼

e. 1/8

7) Roger is relieved that he does not have- LQT7, which affects skeletal as well as cardiac muscle, causing short stature and scoliosis. He is also glad that he doesn't have LQT8, which causes many symptoms, or either of two types that also cause deafness. These other forms of the condition, with more than one symptom, exhibit

a. invariable expressivity.

b. complete penefrance.

c. genetic homogeneity.

d. pleiotropy.

e. phenocopy.

8) The reason that mutations in different genes all cause the same phenotype of extended QT interval on an ECG is that

a. the heart is an extremely complex organ.

b. the genes all encode proteins that affect ion channels essential for maintaining heartbeat.

c. the genes all encode the same protein.

d. the mutations all affect the genes in the same way.

e. the QT interval is highly variable, even within individuals at different times.

9). A phenotypic pattern in a family that could be due to inherited long QT syndrome is

a. sudden cardiac death in one or more young people and individuals who faint easily.

b. many individuals who eat a very fatty diet and are sedentary but do not develop heart disease.

c. many individuals with hypertension.

d. many individuals who suffer heart attacks after age 50.

e. a family with rnany athletes who have very low heart rates because of intense and frequent exercise.

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