UN2006/UN2402 - Corrections
Corrections for the current year are posted on top. Corrections from
previous years are
If you find any errors in outlines, recordings, problem book, or texts, please email Dr. M (dbm2).
Corrections to the outlines for the lectures that are made after the lecture, or after the initial posting of the notes, are marked in blue on the online version; significant changes are listed below.
Last Update: 01/04/2017 05:47 PM
There are no corrections for 2017 yet! They will be posted as soon as needed.
Corrections for 2016
Corrections to -- Problems to Do
For Problem Set 7R -- Do All but skip 7R-1 B, 7R-5 B, 7R-9 B-1, & 7R-10. (Skip questions on TK receptors and the steps of the IP3 pathway.)
For Problem Set 12 R -- Do all but skip 12R-2 & 12R-7 to 12R 12. Note: Low GFR causes renin secretion, which indirectly leads to aldosterone secretion. Circulation is diagrammed on HO 16A; transport in RBC was covered earlier. If necessary, look up any unfamiliar terms.
Corrections to (outlines for) Live Lectures-2016
3/30/16 -- Lecture 12. V-C-3 (part c). The notes say 'splicing factor' when they should say 'poly A addition factor.' The text has been corrected as follows; the parts in blue were added.
c. Mechanism: Site #1 is a 'weak signal' for poly A addition, so it is only used when enough of a particular poly A adding protein (call it protein P) is present. If the level of protein P is below a critical value, the first site is skipped and the second poly A addition site is used.
There is a competition here between splicing out of intron 4 and polyA addition in intron 4. Protein P promotes poly A addition over splicing (of intron 4).
2/4/16 -- Lecture #4. The notes are correct, but I mis-spoke. In a proteoglycan complex, shown on handout 4B, individual proteoglycans are connected to a core GAG by linker proteins. The core is a carbohydrate chain, not a peptide. (See note with * on table in I-B; includes links to picture and refs. to figures in texts.)
2/4/16 -- Lecture #6. The Question from the end of lecture #5 is repeated.
This time it is written correctly. It reads:
(2) Will curve #1 level off at the same value?
The term 'flux' was placed in the wrong place in I-C (Summary of Comparison of Curve #1 & Curve #2). It has been added to the correct place, and a strike out written through the wrong place. The online notes/outlines, both the HTML and PDF versions, have been corrected, and the changes are marked in blue in the notes.
To clarify: Flux = rate of uptake as a function of time = the initial slope of curve #1, not the initial slope of curve #2. In curve #2, flux is plotted against initial concentration of X (outside).
2/2/16 -- Lecture #5-- Question (2) at end of the notes for lecture #5 (In Section
V, A) should read
(2) Will curve #1 level off at the same value?
The online notes, both HTML and PDF, have been corrected, and the change is marked in blue in the notes. The lecture notes were corrected on 2/2 before the am class; if you printed the notes the night before, you need to correct them yourself.
Corrections to Recitation Problems
3/21/16 -- Recitation Problems #8. In problem 33, there are two
answers labeled (b). Delete the second one '
only PDE.' It
is the same as answer (a).
Corrections to Learners' Manual -- 11th edition (2016) See below for corrections to earlier editions
2/8/16 The diagram for problem 2R-10 was missing from page 19. For a scanned copy of page 19, with the diagram, click on this link.
2/14/16 In the diagram for problem 3-4, D some lines should be dotted.
Unfortunately, in the printing, both lines cam out looking solid!! For
the left graph, the top curve should be dotted, and the curve shifted more
to the right should be solid. For the right graph, the top line should be
solid, and the low straight line should be dotted.
here for a corrected version of page 24.
4/12/16 Answer to Problem 14-5, part B. (Page 243.) The answer should be increased methylation, not decreased.
4/12/16 Answer to Problem 14-9, part B. The IPS cells should be specified and determined as will as pluripotent.
Corrections for 2015
Corrections to Live Lectures-15
2/26/15 -- Lecture #11. Some of the references to figure numbers in Becker, and to handout designations, have been updated. The online notes, both HTML and PDF, have been corrected, and all changes are marked in blue in the notes.
4/21/15 -- Lecture #22. Handouts 22A and 22B were incorrectly labeled. (The one labeled '22A' should be '22B' and vice versa.) In the notes, where ever it refers to Handout 22A, you should look at Handout 22B instead, and vice versa. There is no problem with Handouts 22C or 22D.
Corrections to Keys to Exams
Key to Exam #2 -- Problem 4A had a typo. The answer was okay, but there was a mistake in the explanation. Key was corrected on 3/23/15. Corrections (change of P to W) are marked in blue. It is enzyme P that uses the M6P pathway, and enzyme W that does not.
Corrections to Problem Book -- 10th edition (2015) See below for corrections to earlier editions
Problem 3R-5. After part B.ii, instructions for the sketch say
to "put presidin B in the right place..."It should say presidin
Answer to Problem 7R-8, B. The last sentence should read 'GH does stimulate breakdown of glycogen, but not directly.'
Corrections to convert the 9th edition into the 10th
Most of the changes from the 9th edition (2014) to the 10th (2015) are cosmetic.
Those changes are not listed here. Three questions were added --
6-24, 6-25, & 12-23, and the 'old' 6-24 was renumbered 6-26 in the 10th edition. Click here for the added questions (& answers). All other significant changes are listed below.
Clarification to Questions & Answers, in order
of questions -- the italicized words have been added:
Problem 3-7. Parts C & D should now read: :
C. How many localization signals/sequences would you expect to find in the finished protein, once the protein has reached its final destination?
D. Suppose you make radioactive protein in vitro and add it to isolated peroxisomes. You wait a few minutes, long enough for some (but not all) of the protein to enter peroxisomes. Then you isolate proteins from your complete reaction mix = peroxisomes + added protein. You then run the proteins on gels, and look for radioactive bands (as in problem 6). In this experiment, how many radioactive bands do you expect to find on the gel?
Problem 6-24 in the 9th edition is now numbered 6-26. Two new problems were inserted after 6-23.
Problem 9R-8. Parts C & D should now read:
In long QT syndrome, the cardiac contractile cells take longer than normal to
repolarize after an AP – the AP lasts longer than normal. Long QT syndrome could
be caused by a delay in which of the following? (opening of Na+
channels) (opening of K+ channels) (opening of Ca++ channels)
(closing of Na+ channels) (closing of K+ channels) (closing of Ca++ channels) (any of these) (none of these) (several of these, namely ______________________________).
D. In long QT syndrome, a stimulus that has no effect on normal people can cause a premature heart beat – one not triggered by the usual pacemaker -- and generate an irregular rhythm in the heart. In this case, a longer AP causes a premature heart beat. Consider the state of the cardiac muscle membrane. Which of the following is the best explanation for a premature heart beat in this syndrome? (the refractory period lasts longer than the depolarized state) (the depolarized state lasts longer than the refractory period) (the depolarized state is about the same length as the refractory period) (beats me). Explain briefly what the normal situation is, and how it is different in long QT.
Problem 12-17, A & C. Clarifications made to answers. The answers to A & C should read as follows:
A. Less concentrated. The descending limb of loop of Henle concentrates urine by
removing water. If the protein forming the water pores or channels is missing,
the water cannot diffuse out and urine will remain dilute.
From information given, aquaporins must make up pores that allow water to flow across luminal membranes;
#1 must make up the unregulated pores of the descending limb; #2 must make up the pores of the collecting duct that normally respond to ADH. (There are constitutive aquaporins in the BL membrane of the cells, so any water that flows into the cells from the filtrate, will flow out of the cells on the BL side.)
C. #2 should be present in luminal membrane of cells of collecting ducts. Water normally flows out of the filtrate here, concentrating the urine, so pores are needed. If these pores are nonfunctional, urine will remain dilute = diabetes insipidus.
Problem 12-23. New Problem!
Problem 14-8. Changed choices for B so it is clear two choices must be made, not one. Part B should read:
This individual would be a (hermaphrodite) (pseudohermaphrodite), AND probably (XX) (XY) (XXY) (none of the above).
Problem 14-10. Fixed typo in answer. The amino acids in proteins are numbered from the N end, not the C end.
Problem 15R-5. To make it clearer, part A2 has been rewritten as follows:
A-2. Consider the value of
the average EPP triggered by a single pre-synaptic AP. In a normal
person, the average EPP should be: (significantly above threshold)
(significantly below threshold) (close to threshold) (can’t predict).
Corrections for 2014
Corrections to Live Lectures & audios of 2014.
1/29/14 Lecture #3 & Problem 1-20. Terminology: For a multipass protein, each individual section or stretch of polypeptide (transmembrane, extracellular, or intracellular) is usually considered a separate domain. See answer to problem 1-20. All the extracellular or all the intracellular domains may cluster together, but the term 'domain' is not usually used for the entire extracellular (or intracellular) part of the protein. I think this was not stated properly in the live lecture.
2/4/14 Lecture #12. Terminology: In the section on regulation of globin synthesis by heme, the factor that affects translation is called eIF2, not EIF2; eIF2 stands for eukaryotic initiation factor, not elongation factor. (EF# is the usual abbreviation for elongation factors; IF# for initiation factors. )
5/2/14 Lecture #25. The material covered in live lecture 25 is NOT optional. I apologize for any confusion. (It WAS optional in '13 because it was given in study days.) The statement at the end of Lecture #24 was incorrect -- it was an accidental carry over from 2013.
Corrections to Reading List of 2014-- The topics and reading for lectures #7 and #10 were incorrect. They have been fixed. Corrections are blocked in yellow.
Corrections to Becker Text
Becker 6th & 7th ed., fig. 15-11. (c) & 8th ed, fig. 15-10. Becker says human RBC have MT around their edges. According to the experts I consulted, mature human RBC do not contain MT. (They contain a spectrin web instead.) However RBC of other organism do have peripheral MT. Human platelets, but not human RBC, have MT.
Corrections to 9th edition (2014)
4/7/14. Q14-10B. The answer to Q14-10B should state that "convention
numbers every amino acid from the N
terminus in increasing order, ... " The problem book erroneously states
from the C terminus.
If you have the 9th edition, see above for changes to fit the 10th edition.
Corrections to 8th edition (2013)
Changes made to convert the 2013 edition (8th) to
the 2014 edition (9th) are relatively minor, except for Problem Sets 14 &
14A. Here is a summary:
Problem sets 1-3R are the same in the 8th and 9th editions. The only significant differences in problem sets 4 & 4R are a change in terminology. All references to DNase I or micrococcal nuclease have been changed to DNase. In problem set 14, 9 problems have been added. In problem set 14A, two problems (the last two) have been removed. The added problems and the key are posted on CW.
Corrections to older editions of the Problem Book are below.
There were no posted corrections to the Live Lectures of 2013.
Corrections to Live Lectures & audios of 2012.
2/21/12 AM lecture (& on audio). Poly A tails are made from ATP not deoxyATP.
2/16/12 AM lecture (& on audio). When going over the questions on the second PPT slide, I got it backwards, and I said that 'we knew the DNA from the different organs was different.' I meant 'we knew the DNA was not different -- that it was the same.'
1/19/12 AM lecture only. I mis-spoke regrading the picture of arterial endothelial cells shown in class (see PP slides for lect 2 -- slide #2). Endothelial cells lining capillaries, not the endothelial cells lining arteries, have spaces between them that allow small molecules to enter and leave the vessels. Small molecules cannot exit or enter arteries anyway because the endothelial cells lining the arteries are surrounded by layers of smooth muscle. (Capillaries do not have smooth muscle around them.) The cells shown in the picture are from arteries, not capillaries.
Live Lectures & Outlines of '2011
2/15/11 Section III-A of Lecture #8 was updated after the morning lecture. (A few points were accidentally omitted.) For the updated section, click here.
4/12/11 Lecture 17. The equilibrium potential for Na+ is +65 mV, as calculated from the Nernst equation. In the last part of the lecture (III -- Action Potentials) the incorrect value of +50 mV was used when explaining the depolarization that occurs during the AP. This does not affect the basic logic, but the correct value is +65mV.
Lecture 19: The following note was added after the lecture:
Note on refractory periods: There is some disagreement between authorities on the timing of the refractory periods. According to Dr. Firestein, Becker, and most texts, the absolute refractory period comes right after the spike of the action potential. According to some, the absolute refractory period coincides more or less with the spike, and the relative refractory period follows after the spike. All agree about the underlying mechanism. The absolute refractory period corresponds to the time when the Na+ channels are inactivated (so depolarization is not possible). The relative refractory period corresponds to the time when the Na+ channels can be activated, but the voltage gated K+ channels are still open (so depolarization to threshold requires a larger stimulus).
5/3/11 Lecture 25. Early version of lecture said Iressa was a monoclonal Ab. It is not -- it is a small molecule inhibitor. Iressa, Erbitux and Herceptin are all inhibitors of GF receptors, but only the last two are monoclonal antibodies.
Corrections to 2011 Edition (7th ed, re-revised) These are the updates made to convert to the 2013 version (8th ed).
Problem 1-12, part C. Consider filaments attached either directly or indirectly to the inside surfaces, etc.
Problem 1-18 part B. -- Answer. Explanation should say 'cadherins' are single pass, not 'integrins.' Both proteins are single pass, but the problem is about cadherin, not integrin.
Problem 1-22, part B. This problem does not make sense if the fusion proteins were made on the RER and entered the endomembrane system. Therefore the problem says that the proteins are soluble and made in the cytoplasm. (The normal version of ENaC is a TM protein that is released into the endomembrane system, not into the cytoplasm.) The cells could make make soluble fusion proteins in the cytoplasm if the cells were genetically engineered to do so. (This is implied, but not stated, in the problem.) In the actual experiments with fusion proteins described here, the proteins were isolated and then injected into the test cells, not made in the test cells.
Problem 3R-1. Change 'an enzyme converts....' to 'an enzyme catalyzes conversion of......'
Problem 4-11, part A-3. If you get stuck, see Fig. 23-14 in the 8th edition of Becker. This is the same as Fig. 23-17 of Becker (6th or 7th edition).
Problem 4R-1, part B. The problem should refer to the number of types of eukaryotic nuclear RNA polymerases.
Problem 4R-5. Change 300 base pairs to 2000 base pairs. Problem should read: Consider a region of DNA (call it region A) that is 2000 BP before the start of transcription of gene X. In the questions in part B, the chromatin comes from multiple cells, not from a single cell.
Problem 5-8. Hint: Transporters are used to recover salt from perspiration.
Problem 8-20. Part C. The second sentence should read: The ions are at their usual concentrations in the medium (same as the normal extracellular fluid).
Problem 12-22. The star should be on part E -- no star for parts A-D.
Problem 15-17, part A. Handout you need is 25A.
Problem 15-18, Part D-3. Choices should be GGF and GGF receptor not IGF and IGF receptor.
Part D-4. Should refer to the items listed in D-3, not C-3.
Answer to problem 15-18 is labeled '15-8.'
Corrections to 2010 Edition. (If you have the 2009 edition, see this and the corrections above & below.)
Most of the corrections made in 2011 are minor clarifications and/or improvements in formatting and are not listed below. The significant changes are as follows:
Problems 6-6 to 6-9. A handout with the pathways is at http://www.columbia.edu/cu/biology/courses/c2006/handouts/glycogen09.pdf
Problem 4-7, part A-1. -- Answer. Ribosomal proteins moving out of the nucleus as parts of subunits should increase. For individual ribosomal proteins, the answer is 'sts @ zero.'
Problem 14-3. This is the only problem that was completely revised. Here is the updated version & the answer:
Question 14-3. You have 2 DNA samples from two individuals. Call the individuals A & B. The two DNA samples may come from monozygotic twins, or they may come from two cloned individuals -- the nuclear donor and the nuclear recipient of somatic nuclear transfer (SNT). If the DNA samples come from cloning, call the nuclear donor A, and the recipient B.
A. If the two individuals are actually identical twins, & not derived from somatic nuclear transfer (SNT), which of the following would be the same as the DNA of the biological mother and distinguish between the two cases?
(nuclear DNA of both A & B) (mitochondrial DNA of both A & B) (all of the DNA of both A & B)
(the mitochondrial DNA of the clone (B) but not the donor of the nucleus (A))
(the mitochondrial DNA of the donor of the nucleus (A) but not of the clone (B))
(some, but not all of the mito. DNA of A & B) (none of these).
B. If the samples are actually derived from somatic nuclear transfer experiments, which of the following should be the same as the DNA of the egg donor? (nuclear DNA of both A & B) (mitochondrial DNA of both A & B) (all of the DNA of both A & B) (the mitochondrial DNA of the clone (B) but not the donor of the nucleus (A))
(the mitochondrial DNA of the donor of the nucleus (A) but not of the clone (B))
(some, but not all of the mito. DNA of A & B) (none of these).
Answer to 14-3:
A. The important difference between twins and SNT involves the mitochondrial DNA. In the case of the identical twins, the mitochondrial DNA of the kids would match each other and that of the mother (who was the egg donor). If B is a clone of A, B's (the recipient's) mitochondrial DNA would match that of the mother's (the egg donor's) but A's mitochondrial DNA (that of the donor) would not match the mother's. Answer is 'mitochondrial DNA of both A & B.'
B. Only the mitochondria DNA of the cloned individual (B) but not the mitochondria of the donor of the nucleus (A) will match the egg donor. Answer is 'the mitochondrial DNA of the clone (B) but not the donor of the nucleus (A)'.
Corrections to 2009 Edition. If you have the 2010 edition, all these corrections have already been made, and you should see above.
This is what you need if you have the 2009 edition of the problem book. All the changes listed here have already been made in the 2010 edition. This list does not include minor clarifications, mis-spellings that do not obscrue the meaning, or corrections of awkward formating. It only includes changes that alter the meaning.
Cover says "7th edition, revised." It should simply say "7th edition." (7th revised is the 2010 version.)
Problem 1-2. Add to the note at the end: When RBCs are 'resealed' the membranes or fragments that are present form sealed vesicles.
Problem 1-12. Part E should read: Involves close apposition of bilayers from adjacent cells.
Problem 1-22. Add: Assume spectrin A is not the same as RBC spectrin, but is in the same protein family.
Problem 1-23. Answer is not clear enough. It should read:
Complete Explanation: This protein has only one hydrophobic section, which probably makes up a single transmembrane domain. That means that emerin is a single pass protein with 11 amino acids on one side of the membrane, a transmembrane section of 20-30 amino acids (approx.) and the rest of the protein (about 210 amino acids) on the other side of the membrane. Glycosylation happens only to amino acids in domains that are exposed to the lumen of the ER or Golgi; these are the domains that end up on the extracellular side of a plasma membrane protein. Phosphorylation happens inside the cell, in the cytoplasm (not just inside the ER or Golgi), where the kinases and phosphatases are. Since there is one possible glycosylation site and many possible phosphorylation sites, it makes the most sense if the short 11 amino acid tail is on the extracellular side and the large AA domain is intracellular.
The fact that the protein is found in the membrane fraction has nothing to do with the freeze fracture procedure. (See note in problem.)
Problem 2-1. Answer is not clear enough. Explanation of experiment 1 should read:
Experiment 1 shows that the mechanism is passive transport, not active transport, because the final concentration inside the cell = [C2406]in is equal to the external concentration = [C2406]out = about 10mM. Uptake does not affect [C2406]out significantly because the volume of solution on the outside of the cells is so large compared to the volume inside the cells.
Problem 2-6. In this problem, and in the answer, the term 'facilitated diffusion' is used to mean 'carrier mediated transport.' Transport through a channel is considered a separate case.
Problem 2R-10, part F. There is a typo in one of the choices. The 5th choice should be (the region between TM 1 and TM 2) instead of (the region between TM 12 and TM 2).
Problem 3-3. Vesicles that are 'right side out' have the same orientation as whole cells ' what is outside of the vesicle is what would be outside of the cell. These are NOT vesicles formed by RME.
Problem 3-4. Answer to B-1 needs to be updated. (B-2 & B-3 are fine as is.) The answer and the explanation to B-1 should read:
B-1. In the cytoplasm or membrane.
The region coding for section A is the signal sequence. If it is missing, what will happen depends on whether the protein can still bind the SRP or not. If the protein doesn't bind the SRP, it cannot be co-translationally imported into the ER and will remain in the cytoplasm.
It is likely that any hydrophobic sequence, such as C, can bind to the SRP, and act as a signal sequence. In that case, the protein (w/o A) will end up inserted into the ER, using C as both a start and stop transfer sequence (and signal peptide). In this case, the protein will be inserted in the opposite orientation to the usual, so you will have a single pass protein with B (with the free amino end) in the cytoplasm.
If you need a special sequence (to bind the signal recognition particle) not just any old hydrophobic sequence, then region C should not be able to act as a signal sequence and substitute for the missing region A. In that case, the protein will remain in the cytoplasm.
Problem 3-13 -- Answer to Part E. Delete 'see picture for 3-2 part A'. There is no picture!
Problem 3-16. Consider the two plasma membrane proteins described in problem 1-20, not 1-21.
Problem 4-13, part A-1. It should refer to Question 11, not Question 10.
Problem 4R-6. Part B-1, & Answer to parts B and E. The term 'SP' or mito. signal peptide is used to denote the localization signal needed to enter the mitochondrial inner membrane. It would be better to use a different term.
Problem 6-1. It should say 'Consider Protein P described in problem 1-17 (& 3-4)' not 1-18 (&3-2).
Problem 8-4, D, Answer. Delete 'or open voltage-gated'. If you opened the voltage-gated channels, you would cause an AP.
Problem 8-8. In question and answer, A and B refer to the membrane on the post-synaptic side only.
Problem 8-14, part E. x should read: rate of substance moving down axon through the cytoplasm by simple diffusion.
Problem 9R-3, explanation. The nicotinic cholinergic receptor is stimulated by nicotine, not inhibited by it. (Nicotine is an agonist of AcCh, not an antagonist.)
Problem 9R-5. Part A-3. If cell has no alpha 1 receptors, NE should have no effect (unless it binds, although not as well as E, to beta 2 receptors). Question should say assume cell has both types of receptors.
Problem 12-10. Answer to part D. Explanation says 'Aldosterone affects primarily the proximal tubule...' Should say 'distal tubule' not proximal.
Problem 12-14, Answer. Delete part in italics: 'Questions are on next page. 12-14, cont.'
Problem 12-22. Answer to part E. What is labeled 'D-4' is the answer to E-1, and should be inserted before the other answers to part E. What are labeled 'E-1 to E-3' should be relabeled 'E-2 to E-4'.
Problem 12R-16. Answer to part B-3. The lower BP in the kidney will trigger a local response, which is the constriction of the efferent arteriole, or dilation of the afferent. (There is disagreement about which happens here.) The afferent only constricts in response to systemic input which overrides the local response in a case of a big drop in overall BP. (If there is a big drop in overall BP, for example because of sudden blood loss, the systemic input from the sympathetic system reduces GFR. This may temporarily impair kidney function, but is crucial to prevent water loss and restore blood volume.)
Problem 14-1 A. In the table, on the top, it should say ES cells not SC. At the bottom of the table, add the following note: Lens develops from ectoderm.
Problem 14-7. In both the questions & the answers, replace the term 'iES cells' with 'iPS cells.' The terminology has changed.
The first sentence in part B should read: The four genes that are added to the iPS cells code for transcription factors.
In part B-2, the first choice should be (in the nucleus) not (in the nucleolus).
Problem Set 15R. MG is used in problems 2-5 as an abbreviation for myasthenia gravis. See start of 15R-1 for a description of MG.
Corrections to 2007 & 2008 Editions