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A checkpoint component participating in inhibition of Cdc20 as part of the mitotic checkpoint complex.

Re-establishment of a pre-existing methylation pattern following DNA replication.

Madin-Darby canine kidney cell, used in three-dimensional epithelial cyst and polarity assays.

A plant CG methylation maintenance enzyme.

The mitochondrial matrix is the compartment enclosed by the inner mitochondrial membrane, containing mitochondrial DNA, ribosomes and many enzymes. Most citric acid cycle steps occur here; succinate dehydrogenase is membrane-associated. The citric acid cycle supplies NADH for the mitochondrial respiratory chain.^[ref]

Distinguish the location of a chemical reaction from the location of its detection. An external oxygen electrode can report consumption by an intact preparation without entering the mitochondrial matrix. That signal does not locate every intermediate, establish protein targeting or directly count newly formed ATP.

Section of Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. The whole-book authors are Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts and Peter Walter; no independent section-author byline is established. Garland Science published the fourth edition in 2002. NCBI Bookshelf hosts the online text.

Online text: www.ncbi.nlm.nih.gov/books/NBK26837/

Cited passages: Official indexed section text: dideoxy sequencing explanation and Figure 8-36 caption; Figure 8-36 A: normal deoxyribonucleoside triphosphates versus analogues lacking the 3′ hydroxyl group.

Section of Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. The 2002 publication date and author credits belong to the whole book; no separate chapter byline is established. Garland Science publishes the book; NCBI Bookshelf at the National Library of Medicine hosts the text.

Online text: www.ncbi.nlm.nih.gov/books/NBK26878/

Cited passages: Membrane Proteins Can Be Associated with the Lipid Bilayer in Various Ways; Figure 10-17 text and adjacent extraction distinction; cell-surface receptor domains on opposite sides.

Online text: www.ncbi.nlm.nih.gov/books/NBK26841/

Section of Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. The 2002 date and personal author credits belong to the whole book; no separately credited chapter author is established. Garland Science publishes the book; NCBI Bookshelf at the National Library of Medicine hosts the text.

Cited passages: Membrane-bound Ribosomes Define the Rough ER, Figures 12-36 and 12-37; Smooth ER Is Abundant in Some Specialized Cells, Figures 12-38A and 12-38B and calcium-storage paragraphs; Translocation Across the ER Membrane Does Not Always Require Ongoing Polypeptide Chain Elongation; The ER Signal Sequence Is Removed from Most Soluble Proteins After Translocation; In Single-Pass Transmembrane Proteins, a Single Internal ER Signal Sequence Remains in the Lipid Bilayer as a Membrane-spanning α Helix.

Section of Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. Whole-book authors: Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter. No separate chapter author is credited. The 2002 publication date belongs to the whole-book edition. Garland Science publishes the book; NCBI Bookshelf at the National Library of Medicine hosts the online text. No separate section publication or revision date is established.

Online text: www.ncbi.nlm.nih.gov/books/NBK26941/

Cited passages: Molecular Biology of the Cell, 4th edition by Bruce Alberts and others, Transport from the ER through the Golgi Apparatus: Indexed official text: section opening and whole-book citation metadata; Oligosaccharide Chains Are Processed in the Golgi Apparatus; The Golgi Cisternae Are Organized as a Series of Processing Compartments, Figure 13-28 and substrate-order explanation; Transport Through the Golgi Apparatus May Occur by Vesicular Transport or Cisternal Maturation, Figure 13-30 and comparison of nonexclusive models.

Section of Molecular Biology of the Cell, 4th edition by Bruce Alberts and others. The six existing whole-book author credits apply; no separate section byline is established. Garland Science published the fourth edition in 2002; NCBI Bookshelf at the National Library of Medicine hosts the text. No separate section revision date is established.

Online text: www.ncbi.nlm.nih.gov/books/NBK26844/

Cited passages: Lysosomes Are the Principal Sites of Intracellular Digestion, Figure 13–31; Multiple Pathways Deliver Materials to Lysosomes, Figure 13–35 and autophagy paragraph. The inspected text was available through indexed section content; the host restricts direct browsing.

The Wnt ligand participating in the P2-to-EMS interaction during early Caenorhabditis elegans development.

A stator protein contributing to ion-coupled force generation in proton-driven bacterial flagellar motors.

A bacterial mechanosensitive channel that can release solutes during sudden osmotic downshock.

A mutation changes inherited genetic sequence. Under an infinite sites mutation model, every mutation occurs at a previously unmutated position, so mutations below the sample's common ancestor correspond to segregating sites.

More precisely, a mutation changes a genetic nucleotide sequence; in cellular organisms this is a DNA sequence. An altered sequence can be copied by DNA replication into descendant biological cells, changing their genotype whether or not an observable phenotype changes. Inheritance along a cell lineage does not require transmission to an offspring organism. In animals, germline mutations can enter offspring through gametes, whereas somatic mutations remain in body-cell lineages.^[ref]

A DNA lesion is damage to the physical DNA molecule, such as a damaged nucleobase or a broken strand. It need not become a lasting mutation: DNA repair can restore the original sequence. Conversely, a copied nucleotide substitution can leave an ordinary, correctly paired DNA duplex whose sequence differs from the ancestor. The distinction is between a damaged template and a changed inherited message, not simply between harmful and harmless effects.^[ref]

Small mutations include nucleotide substitutions and indels. Larger changes can remove a gene, duplicate a chromosome region or rearrange its order. Genetic recombination can bring existing alleles together without creating a new nucleobase at the exchanged positions; the mechanism and the resulting sequence change are different questions. A molecular description of a mutation, its effect on a gene product and its effect on a phenotype are likewise three separate statements.

For an original consequence ledger, choose the coding strand segment $5^{\prime }\text{-}\mathrm{ATG}\mathrm{TTT}\mathrm{GAA}\mathrm{TAA}\text{-}{3}^{\prime }$ with initiation at the first displayed codon. Use the standard genetic code, the same reading frame and suitable gene expression context throughout. Its messenger RNA has U in place of T, and the predicted amino acid chain is methionine–phenylalanine–glutamic acid residue, followed by a stop codon. This is a constructed coding segment, not an experimentally measured gene.

In the second row, position 6 changes from T to C, replacing TTT by TTC. Both corresponding RNA codons specify phenylalanine, so the predicted chain is unchanged. Changing position 5 from T to C instead gives TCT, whose RNA codon specifies serine. Changing position 7 from G to T gives TAA and therefore a stop codon before the original glutamic acid residue. Each is one nucleotide substitution, but their coding consequences differ. Even preservation of the amino acid chain does not guarantee unchanged gene expression or phenotype.

Insert GGA after ATG to add a glycine codon, or remove the complete TTT codon to remove phenylalanine. Both indels preserve the downstream reading frame because their lengths are three nucleotides. A one-nucleotide insertion at that location instead produces a frameshift mutation; the positional explanation and a worked regrouping appear under frameshift mutation. The ledger illustrates why interpreting a genetic variant requires its position and context, rather than just the label mutation.

Mutation supplies new inherited variation on which natural selection can act. The Luria-Delbrück experiment makes the distinction unusually visible: natural selection reveals resistant descendants, while the timing of a prior mutation determines how many descendants are available to reveal. This connects an invisible change in one biological cell to a visible pattern across cell cultures.

The neck-associated structural element that amplifies conformational changes in the motor domain into displacement.

A class of actin-based cargo motors; well-studied dimeric members coordinate their heads for processive stepping.