Which number represents dna synthesis

Use the following information to answer the questions below. The unlettered circle at the top of the figure shows a diploid nucleus with four chromosomes that have not yet replicated.

There are two pairs of homologous chromosomes, one long and the other short. One haploid set is black, and the other is gray. The circles labeled A to E show various combinations of these chromosomes. Use the data in the accompanying table to answer the following questions. The data were obtained from a study of the length of time spent in each phase of the cell cycle by cells of three eukaryotic organisms designated beta, delta, and gamma.

A gamma contains more DNA than beta B beta is a plant cell and gamma is an animal cell C beta and gamma contain the same amount of DNA D beta cells reproduce asexually.

Nucleotides can be radiolabeled before they are incorporated into newly forming DNA and, therefore, can be assayed to track their incorporation. In a set of experiments, a student—faculty research team used labeled T nucleotides and introduced these into the culture of dividing human cells at specific times.

A infection causes lymphocytes to divide more rapidly B infection causes lymphocyte cultures to skip some parts of the cell cycle C infection causes cell cultures in general to reproduce more rapidly D the presence of the pathogen made the experiments too contaminated to trust the results.

Which of the following aspects of the cell cycle would be most disrupted by cytochalasin B? A spindle attachment to kinetochores B cleavage furrow formation and cytokinesis C spindle formation D cell elongation during anaphase.

A As cells become more numerous, the protein kinases they produce begin to compete with each other, such that the proteins produced by one cell essentially cancel those produced by its neighbor. B As cells become more numerous, the level of waste products increases, eventually slowing down metabolism.

C As cells become more numerous, the cell surface proteins of one cell contact the adjoining cells and they stop dividing. D As cells become more numerous, they begin to squeeze against each other, restricting their size and ability to produce control factors. NEP55 is a protein of the inner nuclear membrane, and L68 is a protein of the nuclear lamina.

What is the most likely role of phosphorylation of these proteins in the process of mitosis? A They are involved in the disassembly and dispersal of the nucleolus.

B They enable the attachment of the spindle microtubules to kinetochore regions of the centromere. C They are involved in the disassembly of the nuclear envelope. D They assist in the movement of the centrosomes to opposite sides of the nucleus. What might explain the association between malignant tumors and chromosomal abnormalities? A Cancer cells are no longer anchorage-dependent. B Cancer cells are no longer density-dependent.

C Cell cycle checkpoints are not in place to stop cells with chromosome abnormalities. D Transformation introduces new chromosomes into cells. Sexual reproduction is not as common, but when it does happen, the haploid gametes have 19 chromosomes. How many chromosomes are in the cells of the underground stems? A Each diploid cell has eight homologous pairs. B The species is diploid with 32 chromosomes per cell. C A gamete from this species has four chromosomes. D The species has 16 sets of chromosomes per cell.

Of the following elements, which do all sexual life cycles have in common? Alternation of generations II. Meiosis III. Fertilization IV. Gametes V. If we choose one of these pairs, such as pair 14, which of the following do the two chromosomes of the pair have in common?

A length, centromere position, and staining pattern only B length and position of the centromere only C length, centromere position, staining pattern, and traits coded for by their genes D They have nothing in common except that they are X-shaped. A the same number of chromosomes and half the amount of DNA. B half the number of chromosomes and half the amount of DNA. These important enzymes can only add new nucleoside triphosphates onto an existing piece of DNA or RNA ; they cannot synthesize DNA de novo from scratch , for a given template.

Another class of proteins fills this functional gap. This particular feature of de novo synthesis is similar to what happens during mRNA transcription. This unique enzyme complex is called DNA primase. The chemical properties of DNA and RNA are quite different, and DNA is the preferred storage material for the genetic information of all cellular organisms, so this reinstallment of a continuous DNA strand is very important.

But it is likely that some connector protein coordinates DNA unwinding and DNA synthesis initiation in eukaryotic cells.

Figure 2: Proteins at the Y-shaped DNA replication fork These proteins are illustrated schematically in panel a of the figure below, but in reality, the fork is folded in three dimensions, producing a structure resembling that of the diagram in the inset b. Focusing on the schematic illustration in a, two DNA polymerase molecules are active at the fork at any one time.

One moves continuously to produce the new daughter DNA molecule on the leading strand, whereas the other produces a long series of short Okazaki DNA fragments on the lagging strand.

Both polymerases are anchored to their template by polymerase accessory proteins, in the form of a sliding clamp and a clamp loader. The helicase exposes the bases of the DNA helix for the leading-strand polymerase to copy. For this reason, the lagging strand polymerase requires the action of a DNA primase enzyme before it can start each Okazaki fragment. Finally, the single-stranded regions of DNA at the fork are covered by multiple copies of a single-strand DNA-binding protein, which hold the DNA template strands open with their bases exposed.

In the folded fork structure shown in the inset, the lagging-strand DNA polymerase remains tied to the leading-strand DNA polymerase. This allows the lagging-strand polymerase to remain at the fork after it finishes the synthesis of each Okazaki fragment. As a result, this polymerase can be used over and over again to synthesize the large number of Okazaki fragments that are needed to produce a new DNA chain on the lagging strand.

In addition to the above group of core proteins, other proteins not shown are needed for DNA replication.

These include a set of initiator proteins to begin each new replication fork at a replication origin, an RNAseH enzyme to remove the RNA primers from the Okazaki fragments, and a DNA ligase to seal the adjacent Okazaki fragments together to form a continuous DNA strand. In eukaryotic cells, these polymerases cooperate with a sliding clamp called p roliferating c ell n uclear a ntigen PCNA.

There may be additional, yet undiscovered, parallel or identical mechanisms or proteins that coordinate DNA unwinding and DNA elongation. A simple yet often effective approach is to find proteins that directly bind to both enzymes.

However, that requires us to understand the molecular architecture of DNA helicase. In eukaryotes, the DNA helicase is comprised of a structural core and two regulatory subunits. Mcm encircles dsDNA Remus et al. Those factors are cell division cycle protein 45 Cdc45 and GINS Go, Ichi, Ni, and San; Japanese for "five, one, two, and three," which refers to the annotation of the genes that encode the complex. Scientists have actually identified two candidate connector proteins that directly bind to both helicase and primase: 1 Mcm10 another Mcm protein that, despite its name, has no functional resemblance to any of the Mcm proteins Solomon et al.

In budding yeast , Mcm10 is essential for replication to occur. However, in these same cells DNA replication can function normally without Ctf4, which means that Ctf4 is not absolutely required Kouprina et al. What about higher eukaryotes? Other experiments in human cells have shown that both proteins seem to be necessary, and work together during replication Zhu, et al.

Scientists are still actively investigating these complex mechanisms. Why is coordination between DNA unwinding and synthesis important? What would happen if you lose this coordination? This would create long regions of vulnerable ssDNA. ATR: an essential regulator of genome integrity. Nature Reviews Molecular Cell Biology 9 , — doi As mentioned above, a checkpoint is a cascade of signaling events that puts replication on hold until a problem is resolved.

How does a cell know that there is a problem with replication? Researchers have recently discovered that, in eukaryotes, the replication protein A RPA is a form of red flag in the cell: when RPA is coating long strands of ssDNA, this signals a checkpoint.

This concept underscores an important feature: presence of ssDNA signals that "something is wrong" and this also holds true for other phases of the cell cycle.

In other words, whether ssDNA is created during replication, or outside of S phase, it will always trigger the checkpoint surveillance system Figure 3. Interestingly, this phenomenon is also present at unprotected telomeres chromosome ends that contain ssDNA Figure 3. What is the mechanism of a red flag, or danger signal that activates a checkpoint?

How does it alert the cell? This starts a that temporarily halts S phase progression. Therefore, ATR is also known as the S phase "checkpoint kinase. ATR kinase acts in several ways to keep the replication process intact. One hypothesis is that phosphorylation of one or several of the Mcm subunits prevents the CMG complex from unwinding more and more DNA. This action effectively stops the process so that it can be repaired before proceeding.

Currently, many researchers are trying to better understand the mechanisms of crosstalk between ATR and the replication machinery Forsburg ; Bailis et al. Nature Reviews Molecular Cell Biology 9 , doi So why would normal cells need ATR? There are other circumstances that cause replication to go awry. One is that the DNA template somehow becomes defective during replication, and causes the polymerase to pause Figures 3 and 4a.

For example, a DNA base can be chemically modified or spontaneously altered. Scientists use the term "stalled forks" for areas of replication forks where DNA polymerization is halted. Little is known about the phosphorylation targets that lie further downstream of Chk1, but when scientists observe Chk1 phosphorylation in cells, they conclude that cells are actively trying to protect replication forks with DNA lesions. What happens when ATR function goes awry? A DSB is a catastrophic event because it ruins the replication fork.

Under these circumstances, cells activate the ATM kinase Figure 4, on the right. It does so by phosphorylating checkpoint kinase 2 Chk2 , a protein that triggers a cascade of phosphorylation events that ultimately result in the repair of the DSB.

Interestingly, when Chk2 triggers events that ultimately repair a DSB, another event also takes place. This event is the phosphorylation of the well-known p53 Caspari This observation is a clue that repairing DSBs may have something to do with preventing the formation of tumors.

Together with a variety of other molecules, ATR and ATM kinases are key factors for the surveillance of DNA replication, and prevent chromosome breakage in dividing cells. However, during repair processes, chromosome fragments can be improperly joined together. Indeed, some scientists consider that such mistakes enable some degree of genetic evolution by creating new and different genetic sequences.

Nevertheless, if even a single cell in our body makes a mistake and fuses DNA fragments to each other that are not supposed to be joined, the rearrangement can be sufficient to deregulate normal cell division. If multiple changes of this type accumulate, then this single cell can eventually turn into a tumor.

In these affected individuals, the cellular surveillance system described above is defective and no longer provides full protection from random events that affect DNA replication.

For example, the name of the ATM protein derives from the affliction that results from a mutated ATM protein: ataxia telangiectasia. In this disease , patients suffer from motor and neurological problems, and they also have what is known as a genome instability syndrome that genetically predisposes them to developing cancer Shiloh With these observations, it may be possible to create new ideas for novel diagnostics and therapies for cancer that specifically track these potent molecules.

The process of DNA replication is highly conserved throughout evolution. Investigating the replication machinery in simple organisms has helped tremendously to understand how the process works in human cells.

Interphase is as term used to include those phases of the cell cycle excluding mitosis and meiosis. Many variants of this generalized cell cycle also exist. Some cells never leave G 1 phase, and are said to enter a permanent, non-dividing stage called G 0. On the other hand, some cells undergo many rounds of DNA synthesis S without any mitosis or cell division, leading to endoreduplication. Understanding the control of the cell cycle is an active area of research, particularly because of the relationship between cell division and cancer.