Errors and Problems in High Yield Cell and Molecular Biology

These last two days have been exhilirating and frustrating. Exhilirating because I’m exposing myself to incredible concepts in Cell Biology that make me want to live in a lab for the rest of my life to discover more; frustrating because of the vessel. Dr. Dudek’s High Yield Cell and Molecular Biology (2nd Ed. 2007) is riddled with errors in grammar, spelling, punctuation, etc. As an English marm, I find this incredibly distracting. Further, there are a number of times where the book is not internally consitent (i.e. page 10 contradicts page 20), presents concepts in obfuscating ways (this may just be me being dense), or makes factual errors.

I didn’t schedule the time to spend a few hours each day trying to decipher conflicting statements. Though I found sections of this book amazing, the confusing tradeoffs weren’t worth it. If I were to do it all over again, I would not buy this book.

But if you did buy this book and just searched for “errors in High Yield….” then what follows is what I’ve found. This comes from an email I composed to Dr. Dudek, notifying him of the problems. You have to appreciate an author that gives out their email address like that.

Comments are arranged by Chapter-Page-Section. Important errors are underlined and emboldened. Please escuse my hubris:

Chapters 1-13 (out of 26)

  1. The Cell Membrane
    1. P.6, A.13.17: Abbreviation “DST of the loop of Henle” not explained. I knew this term as Thick Assending Limb and not Distal Straight Tubule.
    2. P.7, B: “across the membrane and [verb?] generally called ion channels.”
    3. P.10, B.2: Title: “Transmitted-gated ion channels” should be “TransmitteR-gated…”
    4. P.11, B.2.c: “..the gate is opened and the influx and Na+ and efflux..” “And” should be replaced with “of”.
    5. P.11, B.2.d: “Purinergic 2x” conflicts with P.16, E: “Purinergic 1,2y” These may be different; I raise it only because both are found on “peripheral terminals of nociceptive neurons.”
    6. P.13 is amazing, by the way.
    7. P.14, C: “..trimer with GDP bound to the [alpha] chain..” The [alpha] should have a “q” after it.
    8. P.15, B: You refer to the actions of both Beta-agonists and Beta-antagonists as having “(positive chronotropism; B1 effect).” This is confusing. As I’ve seen it, these drugs are typically described as being “negatively or positively chronotropic” for antagonists and agonists, respectively.
    9. P.16, C: You have the PLc pathway as producing a “[down arrow/decrease in] IP3 + DAG” when it actually produces an increase in IP3 and DAG.
    10. P.18, P.4: last sentence: “…receptor antagonists and are used to [verb?] opioid toxicity…”
    11. P.21, VII: last sentence: “When LDL … binds to the LDL receptor, receptor-mediated endocytosis [verb?] in the following steps:”
    12. P.21, VII.C: You abbreviation “HNG-CoA reductase” should be “HMG-CoA reductase.”
  2. Cytoplasm and Organelles
    1. P.23, I.E: “…and a DNA-binding region that activate gene…” It should be “activates.”
    2. P.30, C.2: last sentence: “The absence of glucose-6-phosphatase enzyme in skeletal muscle prevents the degradation of glycogen to free glucose,” while certainly correct, is confusing if you don’t already know that this absence is normal, and that no skeletal muscle has this enzyme. Without this context, I would have read this as being a disease state. I think it could be reworded:
      1. “Skeletal muscle lacks glucose-6-phosphatase, thereby committing the stored glycogen to be used by the muscle in glycolysis.”
    3. P.32, Figure 2-2, O: “High magnification of a mitochondria with tubular cristae.” The significance of mitochondrial tubular cristae in steroid-secreting cells was not addressed in this chapter.
  3. Nucleus
    1. Figure 3-2 was really helpful
  4. Protein Synthesis
    1. P.38, II.A: “DNA sequences that flank the gene sequence at the 5′ end of the template strand are called upstream sequences. DNA sequences that flank the gene sequence at the 3′ end of the template strand are called downstream sequences.” This is not correct and conflicts with every mention to follow of upstream/downstream sequences, i.e. P. 95-97.
      1. Template strand: upstream: 3′ of gene
      2. Template strand: downstream: 5′ of gene
      3. Non-template strand: upstream: 5′ of gene
      4. Non-template strand: downstream: 3′ of gene
    2. P.43, Figure 4-3: For some reason the last drawn ribosome has the two subunits separated.
    3. P.44, Figure 4-4, A(3): After giving the translation of each codon-to-amino acid sequence, you omit that UAA codes for STOP. I think that this should be included for completeness.
  5. Chromosomal DNA
    1. P.45, II.B: “…impart a positive charge to the proteins that enhances it binding to…” It should be “..enhances its binding to…”
    2. P.46, II.C: “(an enzyme can pass on DNA double..” This should be “can pass one DNA double”
    3. P.46, II.D: “During metaphase of mitosis, [subject?] can become…”
    4. P.46, III: last sentence: “Microtubules produced the by centrosome…” should be “by the centrosome“.
  6. Numerical Chromosomal Abnormalities
    1. P.54, II.B: You state that chimerism is the “reverse of twinning.” While I understand what you are going for by way of analogy, genetically-speaking, chimerism is not the reverse of twinning and this analogy is potentially confusing.
    2. P. 57, Figure 6-3, (A,B): When describing Patau syndrome, you list “fingers flexed and overlapping” as a key feature. This is a key feature of Edwards syndrome.
    3. P.61, III.I. The notation for each of the multiple myeloma translocations is out of order, i.e. t(14;4), t(14;6), t(14;11) should instead be t(4;14), t(6;14), t(11;14).
    4. P.66, VII.A: last sentence: “…encodes for DNA polymerase eta[?] that is involved…”
    5. P.66, VII.C: missing comma between “hypogonadism” and “microcephaly”
  7. Structural Chromosomal Abnormalities
  8. Chromosome Replications and DNA Synthesis
  9. Meiosis and Genetic Recombination
    1. P.82, Figure 9-2, A: This figure is confusing because the end product shows only a swapped intermediate sequence and does not show how the remainder of the chromosome arms can be switched between the two chromosomes using a Holliday junction. This site has a very good demonstration that might be adapted to fit the space of this page.
  10. The Human Nuclear Genome
    1. P.87, III.F-H: These descriptions are great, but why is there no reference to Figure 12-3 (P.104) which shows how each of these works? Most of the information here is also repeated word-for-word in chapter 12. I think moving Figure 12-3 into this chapter and then (instead of repeating the information) simply referencing III.F-H when the time comes in chapter 12 would help.
    2. P.89, V.C: “Simple variable number tandem repeats (VNTR) polymorphisms called microsatellite DNA or SSR polymorphisms … are typically found in microsatellite DNA.” This is self-referencing and confusing. I don’t know what you mean when you say that microsatellite DNA is typically found in microsatellite DNA.
    3. P.91, Figure 10-2 (F): It was my understanding that two transposons, flanking a gene, carrying out gene transfer required the “cuts” to be on the outermost edges of the transposons, thereby incorporating both transposons with the gene into the new location. This figure shows the gene being transferred without accompanying transposons.
  11. The Human Mitochondrial Genome
  12. Control of Gene Expression
    1. P.07, II.B.3: “CREB (cAMP response element binding protein) binds to the CRE in response to elevated cAMP levels in the cell caused by a protein hormone binding to a G protein-linked receptor and thereby induces gene expression.” I found this sentence very confusing. Because the sequence of events is very linear, I think a more linear sentence is appropriate:
      1. “A cell signal produced by a G protein-linked receptor (resulting in an increase in cAMP) triggers CREB (cAMP response element binding protein) to bind to CRE.
    2. P.100, Figure 12-2 (A): The drawing of the folded Homeodomain protein has the COOH terminus and NH2 terminus switched.
    3. P.101, V.D: “There a[are?] several human genes that [verb?] two or more alternative promoters which…”
    4. P.101, V.D: “Alternative promoters start transcription from different versions; the first exon, which is then spliced into a common set of downstream exons, which produce an isoform of the same molecular weight.” This should say:
      1. “Alternative promoters start transcription from different versions of the first exon, which is then spliced into a common set of downstream exons, and produce isoforms of the same molecular weight.”
    5. P.101,V.D: “…but different amino acid sequences in the NH2-terminal end.” This should say “…but different amino acid sequences in the COOH-terminus.”
    6. P.102, V.G: “…~20% of the total genes on the X chromosome escape inactivation. These ~20% inactivated genes include…” This is contradictory. This should say “These remaining active genes include…”
    7. P.103, VI.D.4: “Glucose and lactose(+)” should be “Glucose(-) and lactose(+).”
    8. P.104, Figure 12-3 (D): “Note that each alternative promoter uses in own first exon” should be “promoter uses its own.” “The size of the dystrophin isoforms are show” should be “shown.”
  13. Mutations of the DNA Sequence
    1. P.107 III: You describe nonsense mutations as producing “non-functional (truncated) proteins” and frameshift (or DNA splicing) mutations as producing “non-functional (“garbled”) proteins.” According to the mechanisms described, both frameshift and DNA splicing mutations can produce “garbled” and truncated proteins.
    2. P.107-108, III.F-G: After stating that Translocational and Unstable Expanding Repeat Mutations have been previously covered (and you reference them), you reprint the text. I think you could save this space.
    3. P.109, IV.A: No examples given of haploinsufficiency but several examples given for gain of function mutations. I would have liked to read about a few of them.
    4. P.110, IV.B: “In order for gain of function mutations to become clinically relevant, the individual needs to be heterozygous (i.e. Rr).” Because homozygotes are not excluded (through inheriting these traits), I think it is more correct to say that:
      1. In order for gain of function mutations to become clinically relevant, the individual needs to have at least one copy of the gene (i.e. Rr or rr).
    5. P.110, IV.B.1: “Pittsburgh variant is a missense mutation in the [alpha]1-antitrypsin protein that produces a gain of function mutation known as the Pittsburgh variant.” This is confusing. I do not know what you mean to say that Pittsburgh variant produces Pittsburgh variant. “…methionine358 in the reactive center acts a bait for…” should be “…acts as bait…”
    6. P.110, V: “Fourth, a polymorphism is the occurrence of two or more alleles at a specific locus in a frequencies greater than can be explained by mutations alone (a polymorphism does not cause a genetic disease).” I found this explanation confusing and it does not mention that it is judged on the characteristics of the population that carries it. I think that the Oxford definition is less confusing:
      1. The occurrence of two or more alleles for a given locus in a population where at least two alleles appear with frequencies of more than 1%.
    7. P.110, V.A.2: When writing about Unequal Sister Chromatid Exchange, you write that: “…cleavage and rejoining of sister chromatids occurs at different positions on the maternal chromosome usually within a region of tandem repeats.” followed by the exact same sentence, changing only “maternal” to “paternal.” I think you should change this into one sentence, reading:
      1. …cleavage and rejoining of sister chromatids occurs at different positions on the (maternal/fraternal) chromosome usually within a region of tandem repeats.”
    8. P.111, V.A.3: When describing replication slippage, you don’t mention that the strand that is slipping either “forward” or “backwards” refers to the parent or daughter strand (respectively). You also don’t mention that the insertions and deletions only affect one arm of the sister chromatid. I think you should expand the description of replication slippage and include something similar to this figure (click to enlarge) that illustrates that the templates are unchanged, therefore there is a 50/50 chance that no insertion or deletion will be passed on.
    9. P.114, Figure 13-1 (G): “PNA splicing” should be “RNA splicing”

Return to USMLE Step 1 page.

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2 Responses to Errors and Problems in High Yield Cell and Molecular Biology

  1. jay says:

    Any word from Dr. Dudek on making these corrections for the next edition?

  2. That is a huge bonus in the dieting recipes process too difficult to stick
    to your diet on a regular basis. The first thing you need to properly smell the tastants.

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