The cell cycle is the process by which a cell grows, duplicates its DNA, and divides into identical daughter cells. Cell cycle duration varies according to cell type and organism. In mammals, cell division occurs over a period of approximately twenty-four hours.
In multicellular organisms, only a subset of cells go through the cycle continuously. Those cells include the stem cells of the hematopoietic system, the basal cells of the skin, and the cells in the bottom of the colon crypts . Other cells, such as those that make up the endocrine glands, as well as liver cells, certain renal (kidney) tubular cells, and cells that belong to connective tissue, exist in a nonreplicating state but can enter the cell cycle after receiving signals from external stimuli. Finally, postmitotic cells are incapable of cell division even after maximal stimulation, and include most neurons, striated muscle cells, and heart muscle cells.
The cell cycle is functionally divided into discrete phases. During the DNA synthesis (S) phase, the cell replicates its chromosomes. During the mitosis (M) phase, the duplicated chromosomes are segregated, migrating to opposite poles of the cell. The cell then divides into two daughter cells, each having the same genetic components as the parental cell. Mammalian cells undergo two gap, or growth, phases (G1 and G2). G1 occurs prior to the S phase, and G2 occurs before the M phase.
Control of the Cycle
During the G1 and G2 phases, cells grow and make sure that conditions are proper for DNA replication and cell division. During the G1 phase, cells monitor their environment and determine if conditions, including the availability of nutrients, growth factors and hormones, justify DNA replication. The decision to initiate replication is made at a specific "checkpoint" in G1 called the "restriction point."
The processes of DNA replication and mitosis, and intervening events during the cell cycle, occur in a highly ordered and specific manner. A complex network of proteins ensures that these events occur at the proper times. Intracellular and extracellular signals block cell-cycle progression at checkpoints if certain events have not yet been completed. After the restriction point, the cell is committed to replicating its genome and dividing, completing one round of the cell cycle. If, prior to the restriction point, cells sense inadequate growth conditions or receive inhibitory signals from other cells, they enter G0 (G-zero) phase, also called quiescence. In the G0 phase, they are maintained for prolonged periods in a nondividing state. If cells sense such conditions after the restriction point, they complete the current round of the cell cycle and exit to G0 during the subsequent G1 phase. The G2 phase is shorter than G1, but it, too, consists of important mechanisms that control the completion and fidelity of DNA replication and that prepare the cell for entry into mitosis. Whereas some conditions cause cells to enter the G0 phase, others trigger apoptosis . One such signal that may trigger apoptosis is if a cell's DNA has undergone significant damage.
After the restriction point, at the transition from the G2 to the M phase, another checkpoint occurs. Mitosis is prevented if DNA damage has occurred or if genomic replication is not complete. The final key checkpoint occurs at the end of mitosis, when the cycle stops if chromosomes are not properly attached to the mitotic spindle.
Proteins That Regulate the Cycle
The mammalian cell cycle control system is regulated by a group of protein kinases called cyclin-dependent kinases (CDKs). These proteins catalyze the attachment of phosphate groups to specific serine or threonine amino acids in a target protein. The phosphate groups alter the target protein's properties, such as its interaction with other proteins. (The alteration of protein activity by the attachment of phosphate groups occurs frequently in cells.)
CDKs are called "cyclin-dependent" because their activity requires their association with activating subunits called cyclins. While the number of CDKs in a cell remains constant during the cell cycle, the levels of cyclins oscillate. There are G1 cyclins, S-phase cyclins, and G2/M cyclins, each of which interact differently with CDK subunits to regulate the various phases of the cell cycle. CDKs can also associate with inhibitory subunits called CDK inhibitors (CKIs). In response to signals that work against proliferation, such as growth factor deprivation, DNA damage, cell-cell contact inhibition and lack of cell adhesion, CKIs cause the cell cycle to halt.
By the end of 2001, many structurally related cyclins (A1, A2, B1, B2, B3, B4, B5, C, D1, D2, D3, E1, E2, F, G1, G2, H, I, L, and T) and nine CDKs (CDK1 to CDK9) were identified in mammalian cells. Complexes of cyclin D and CDK4, as well as complexes of cyclin D and CDK6, operate during the G1 phase. Complexes of cyclin A and CDK2, as well as complexes of cyclin E and CDK2, act during the transition from the G1 to the S phase. Complexes of cyclin A and CDK1, as well as cyclin B and CDK1, function during the transition from the G2 to the M phase.
Active complexes of cyclins and CDKs exert their biological effects by phosphorylating proteins. During the G1 phase, a major target of cyclin/CDK complexes is the retinoblastoma protein (pRb). pRb is a growth-suppressing protein whose activity is controlled by whether or not it is phosphorylated.
When pRb is in the dephosphorylated form, during the G0 phase and early in the G1 phase, it is active. pRb exerts its growth-suppressing effects by binding to many cellular proteins, including the transcription factors of the E2F family (Figure 1). E2F transcription factors regulate the expression of numerous genes that are expressed during G1, or at the transition from the G1 to the S phase, to initiate DNA replication.
pRb that is bound to an E2F transcription factor inhibits the transcription factor's activity. Following phosphorylation by cyclin/CDK complexes, pRb dissociates from E2F, allowing the transcription factor to bind DNA sequences and activate the expression of genes necessary for the cell to enter the S phase. Cyclin D1/CDK4 complexes phosphorylation of pRb during the middle of the G1 phase. They allow for subsequent phosphorylation of pRb by additional cyclin/CDK complexes that act later in the cell cycle.
Two families of CKIs have been identified, based on their amino acid sequence similarity and the specificity of their interactions with CDKs. One of the families of CKIs, the INK family, includes four proteins (p15, p16 p18 and p20). These CKIs exclusively bind complexes of cyclin D and CDK4, as well as complexes of cyclin D and CDK6, to block cells that are in the G1 phase of the cell cycle. The other family of CKIs, the Cip/Kip family, consists of three proteins (p21, p27, and p57). These inhibitors bind to all complexes of cyclins and CDKs that function during the G1 phase and during the transition from the G1 to the S phase. They act preferentially, however, to block the activity of complexes containing CDK2.
Deregulation and Cancer
Deregulation of cell cycle control proteins plays a key role in the development of cancer. Overactivation of proteins that favor cell cycle progression, namely cyclins and CDKs, and the inactivation of proteins that impede cell cycle progression, such as CKIs, can result in uncontrolled cell proliferation.
In human tumors , it is genes encoding the proteins that control the transition from the G1 to the S phase that are most commonly altered. These genes include those for cyclins, CKIs, and pRb. Such mutations overcome the inhibitory effects of pRb on the cell cycle, causing cells to have a growth advantage. In some cancers, this occurs after the direct mutation of the pRb gene, resulting in the protein's loss of function. In a larger set of cancers, pRb is indirectly inactivated by the hyper-activation of CDKs. This may result from over expression of cyclins, from an activating mutation in CDK4, or from inactivation of CKIs.
There is much evidence to suggest that cyclins can act as oncogenes to induce cells to become cancerous. In particular the G1 cyclins, cyclin D1, and cyclin E have been implicated in the development of cancer. Over-expression of the cyclin D1 protein is frequently detected in human breast cancer, and increasing evidence suggests that cyclin E overexpression plays an important role in the pathogenesis of breast cancer.
CKIs antagonize the function of cyclins, and considerable evidence suggests that these proteins function as tumor suppressors. CKI function is often altered in cancer cells. The gene encoding p16, a protein that belongs to the INK family of CKIs, is mutated, deleted, or inactivated in a large number of human malignancies and tumors. Such alterations prevent the inhibition of cyclin D/CDK4 and cyclin D/CDK6 complexes during G1.
Decreased expression of p21 and p27, proteins that belong to the Cip/Kip family of CKIs, also has been demonstrated in numerous human tumors. In contrast to the genetic mutations observed with p16, the decrease in p27 levels in tumors is due to enhanced degradation of the p27 protein. One of the proteins required for the degradation of p27, Skp2, has oncogenic properties. Skp2 over expression is observed in several human cancers and likely contributes to the uncontrolled progression of the cell cycle by increasing the degradation of p27. Understanding of the fine details of cell cycle regulation is likely to lead to specific cancer therapies targeting one or more of these important proteins.
see also Apoptosis; Cancer; Cell, Eukaryotic; Meiosis; Mitosis; Oncogenes; Replication; Signal Transduction; Tumor Suppressor Genes; Transcription Factors.
and Michele Pagano
Goldberg, Alfred L., Stephen J. Elledge, and J. Wade Harper. "The Cellular Chamber of Doom." Scientific American 284, no. 1 (2001): 68-73.
Gutkind, J. Silvio, ed. Signaling Networks and Cell Cycle Control. Totowa, NJ: Humana Press, 2000.
Murray, Andrew, and Tim Hunt. The Cell Cycle: An Introduction. Oxford, U.K.: Oxford University Press, 1993.
Pagano, Michele, ed. Cell Cycle Control. New York: Springer-Verlag, 1998.
Weinberg, Robert A. "How Cancer Arises." Scientific American 275, no. 3 (1996): 62-70.
The cell cycle is the ordered series of events required for the faithful duplication of one eukaryotic cells into two genetically identical daughter cells. In a cell cycle, precise replication of deoxyribonucleic acid (DNA) duplicates each chromosome . Subsequently, the duplicated chromosomes separate away from each other by mitosis , followed by division of the cytoplasm , called cytokinesis.
These monumental transformations in the chromosomes are accompanied by general cell growth, which provides enough material of all sorts (membranes, organelles , cytosol , nucleoplasm) required for the resultant doubling of cell number. This cycle continues indefinitely in specialized cells called stem cells, found in skin or bone marrow, causing constant replenishment of cells discarded by natural physiological processes.
Repetition of the cell cycle may produce a clone of identical cells, such as a colony of baker's yeast on a petri dish, or it may be accompanied by intricate changes that led to differentiation into distinctive cell types, or ultimately to the development of a complex organism. In all cases, the DNA sequence of each cell's genome remains unchanged, but the resultant cellular forms and functions may be quite varied.
Stages of the Cell Cycle
From the viewpoint of chromosomes, four distinct, ordered stages constitute a cell cycle. DNA synthesis (S) and mitosis (M) alternate with one another, separated by two "gap" phases (G2 and G1) of preparation and growth. Though a generic cell cycle possesses no definitive starting stage, the term "start" of the cell cycle has nonetheless been given to the initiation of chromosomal DNA replication or synthesis. During S phase, every chromosome replicates to yield two identical sister chromosomes (called chromatids ) that remain attached at their kinetochores. G2, a period of apparent chromosomal inactivity, follows S phase. In G2, cells prepare for the dynamic chromosomal movements of mitosis. In mitosis, the duplicated chromosomes separate into two equal groups through a series of highly coordinated events. First, condensed sister chromatids attach to the mitotic spindle at the center of the cell. The mitotic spindle, a fanlike array of microtubules, mediates the separation of all sister chromatid pairs as the chromatids, now called chromosomes, synchronously move to opposite poles of the cell.
Cytokinesis follows, in which the cytoplasm pinches apart and two new intact daughter cells are formed, each with the correct complement of chromosomes. G1, a phase of cellular growth and preparation for DNA synthesis, occurs next. Thus a cell cycle proceeds from S to G2 to M to G1, and the two new cells' cycles continue to S and onward through the same series of stages. Cells that no longer undergo mitosis are said to be in G0. Such cells include most neurons and mature muscle cells.
Both internal and external inputs trigger molecular events that regulate normal progress through the stages of the cell cycle. The precisely choreographed movements of chromosomes during mitosis provide one example of this intrinsically faithful, careful regulation. The apparent simplicity of the particular alignment, division, and locomotion of chromosomes in each normal cell division belies the many levels of regulation that guarantee such precision. For example, without complete and proper DNA replication, the events of mitosis are not initiated. This control of cell-cycle order is maintained through an intracellular "checkpoint" that monitors the integrity and completion of DNA synthesis before authorizing the initiation of mitosis. This S-phase checkpoint responds to various forms of DNA damage, such as single-and double-strand breaks in the DNA backbone or incorporation of unusual nucleotides , and halts the progression of the cell cycle until effective repairs have occurred. The S-phase checkpoint also responds to stalled DNA replication forks, making the cell cycle pause until replication is completed. Ted Weinert and Lee Hartwell were the first to report experimental evidence of such a cell-cycle checkpoint in 1988. Since then, checkpoints have been discovered that regulate many aspects of cell-cycle progression in all organisms studied. Initiation of DNA synthesis, assembly and integrity of the mitotic spindle, and chromosome attachment to the mitotic spindle are all regulated by checkpoints. Mutations in checkpoint genes can lead to cancer, because of the resultant deregulation of cell division.
Regulation by CDK Proteins
Remarkably, the coordinated transitions between cell cycle stages depend on one family of evolutionarily conserved proteins , called cyclin-dependent kinases . Cyclin-dependent kinases (CDKs) act as oscillating driving forces to direct the progression of the cell cycle. Each CDK consists of two parts, an enzyme known as a kinase and a modifying protein called a cyclin. Kinases are regulatory enzymes that catalyze the addition of phosphate groups to protein substrates . Adding one or more phosphate groups to a substrate protein can change that substrate's ability to do its cellular job: One particular substrate may be inhibited by such a modification, while a different substrate may be activated by the same type of modification. Cyclins, so named because their activity cycles up and down during the cell cycle, restrict the action of their bound kinase to particular substrates. Together, the two integral parts of a CDK target specific cellular proteins for phosphorylation , thereby causing changes in cell-cycle progression.
Each CDK, consisting of a particular kinase bound by a particular cyclin, directs a critical transition in the cell cycle. For example, one CDK controls the initiation of DNA synthesis, while another CDK controls the onset of mitosis. Inactivation of the mitotic CDK is necessary for a subsequent cell-cycle transition, when cells exit mitosis and proceed to G1. CDKs are also the ultimate targets of most cell-cycle checkpoint activity. So that all cell-cycle events occur at the proper time during each cell cycle, CDK activity itself is tightly controlled by regulating the activity of every cyclin. Each cyclin is active only periodically during the cell cycle, with its peak of activity limited to the period during which it is needed. Regulated transcription of cyclin genes and regulated degradation of cyclin proteins provides this oversight.
In addition to intrinsic controls exerted by CDKs and checkpoints, many external controls affect cell division. Both normal and abnormal cell cycles can be triggered by such extrinsic controls. For example, the hormone estrogen affects the development of a wide variety of cell types in women. Estrogen exerts its effects on a receptive cell by binding to a specific receptor protein on the cell's nuclear membrane. By binding to an estrogen receptor, estrogen initiates a cascade of biochemical reactions that lead to changes in the cell-cycle program. Normally, estrogen moves cells out of a resting stage into an active cell cycle.
In a different context, however, even normal levels of estrogen encourage the growth of some forms of breast cancer. In these cases, estrogen increases the speed with which the cancerous cells complete their cell cycles, leading to more rapid growth of the tumor. The most effective current drug therapies for such breast cancers block the estrogen receptor's estrogenbinding ability, making cells unresponsive to estrogen's proliferation signal. Thus, while estrogen itself does not cause breast cancer, it plays an important role in stimulating the growth of some cancers once they initiate by other mechanisms, such as by an unregulated CDK or a defect in a cell-cycle checkpoint.
see also Control Mechanisms; Genetic Control of Development; Hormones; Oncogenes and Cancer Cells; Signaling and Signal Transduction
Wendy E. Raymond
Hartwell, Leland H., et al. Genetics: From Genes to Genomes. New York: McGraw-Hill, 2000.
Hartwell, Leland H., and T. A. Weinert. "Checkpoints: Controls That Ensure the Order of Cell Cycle Events." Science 246 (1989): 629–634.
Murray, Andrew, and Tim Hunt. The Cell Cycle: An Introduction. New York: W. H. Freeman and Company, 1993.
During the cell cycle, cells grow, double their nuclear deoxyribonucleic acid (DNA) content through chromosome replication, and prepare for the next mitosis (chromosome separation) and cytokinesis (cytoplasm separation). In effect, the cell cycle is the proliferating cell's life history. Cells spend most of their time in interphase, the period between divisions, acquiring competence for division. For example, in the higher plant Arabidopsis thaliana at 23°C, meristematic cells are in interphase for eight hours but are in mitosis for only thirty minutes.
The Phases of the Cell Cycle
The cell cycle is commonly described as having four phases: M (mitosis), Gap 1 (postmitotic interphase), S-phase (period of DNA synthesis), and Gap 2 (postsynthetic interphase). Gaps 1 and 2 were initially thought to be resting stages between mitosis and S-phase. This description is a misnomer because numerous genes regulate cell growth in these phases. Appropriately, these terms became abbreviated to G1 and G2. Moreover, networks of cell cycle gene products constitute molecular checkpoints that in G1 determine whether a cell is competent to replicate its chromosomes during S-phase, and that in G2 sense whether the cell is ready to partition its chromatids during mitosis. Uniquely in plant cells, in late G2 an array of microtubules known as the preprophase band appears and chromosomes separate in a plane perpendicular to it.
Only in mitosis do chromosomes become visible by light microscopy; each one appears as two sister chromatids constricted at a specific point along their length, the centromere. At mitosis, a diploid parent cell passes through four phases: prophase, metaphase, anaphase, and telophase. During late prophase, the nuclear envelope disintegrates and spindles of microtubules span the cell. Unlike animal mitosis where the spindles attach to centrioles (and associated polar asters), there is no obvious anchoring structure for higher plant spindles. This led to the botanical term "anastral cell division." At metaphase, the chromosomes align at the cell's equator and attach to mitotic spindles via kinetochores, discs of structural protein that also bind to the centromere of the chromosome. During anaphase, sister chromatids are pulled apart and move to opposite ends of the cell. In telophase, nuclear envelopes reform around each new diploid set of chromosomes followed by cytokinesis when a new wall forms between sibling cells. Cytokinesis requires the formation of a cell plate or phragmoplast that spans the cell center, and becomes dense with vesicles from the Golgi complex (also called the Golgi apparatus). The plasma membrane and the membrane surrounding the phragmoplast fuse, resulting in separation of the sibling cells. On the phragmoplast, cellulose forms the fibrillar component of the cell wall while hemicelluloses and pectins are added as a matrix. Trapped in the primary cell wall are cytoplasmic strands and microtubules that become plasmodesmata, the cytoplasmic connections between the new cells.
Most knowledge about regulatory cell cycle genes comes from studies of yeasts and vertebrate cells, but the molecular landscape of the plant cell cycle is being identified. In fact, an important discovery about the cell cycle stemmed from work on plant cells in the 1960s by Jack Van't Hof at the Brookhaven National Laboratory in New York. He discovered that when cultured pea root tips were deprived of carbohydrate, meristematic cells stopped dividing and arrested in either G1 or G2. If sucrose and inhibitors of protein synthesis or adenosine triphosphate (ATP ) synthesis were then added to the medium, the cells continued to arrest in G1 or G2 despite nutrient availability. With confirmatory data from other species, in 1973 Van't Hof published his principal control point hypothesis: that there are two major control points of the cell cycle, one at G1/S and the other at G2/M, both of which are dependent on adequate nutrients, the generation of energy, and protein synthesis. Discovery of the proteins synthesized at these transitions and the genes that encode them occurred in the 1980s. Paul Nurse at the Imperial Cancer Research Fund (ICRF) in London discovered that a fission yeast cell division cycle (cdc) gene, cdc2, was absolutely required for the G2/M and G1/S transitions. Cdc2 encodes a protein kinase, an enzyme that catalyzes substrate phosphorylation. Although the kinase (also called p34 because its molecular weight is 34 kilodaltons), is not fully understood, it can phosphorylate lamin proteins that line the inside of the nuclear envelope. Notably, phosphorylated lamins become unstable, leading to nuclear envelope breakdown. Presumably, p34 drives a cell into mitosis at least partly because it phosphorylates lamins. Genes equivalent to cdc2 have been discovered in humans, frogs, insects, fish, and higher plants.
How does mitosis stop so abruptly when two siblings enter G1, even though p34 is still present? This puzzle was partly solved by Tim Hunt at the ICRF laboratories. A protein extract injected into immature frog oocytes caused them to undergo meiosis prematurely. Hunt noticed one protein in the extract that increased in concentration during the cell cycle but disappeared suddenly at the M to G1 phase transition. It was called cyclin. Data from the fission yeast and frog systems indicated that p34 depends on cyclin for its phosphorylating activity. In fact, p34 and cyclin bind together from late G2 until late mitosis and then, suddenly, cyclin is degraded, p34 stops working, and mitosis ends. Plant-like cyclins have also been identified in various higher plants including Arabidopsis, alfalfa, and rice, reflecting remarkable conservation of the key cell cycle genes among unrelated organisms.
see also Cells; Cells, Specialized Types; Meristems.
Alberts, Bruce, D. Bray, J. Lewis, M. Raff, K. Roberts, and J. D. Watson. The Molecular Biology of the Cell, 3rd ed. New York: Garland, 1994.
Eukaryotic organisms encompass a range of organisms, from humans to single-celled microorganisms such as protozoa . Eukaryotes are fundamentally different from prokaryotic microorganisms, such as bacteria , in their size, structure and functional organization.
The oldest known eukaryote fossil is about 1.5 billion years old. Prokaryote fossils that are over 3 billion years old are known. Thus, prokaryotic cells appeared first on Earth. The appearance of eukaryotic cells some 1.5 billion years ago became possible when cellular function was organized into regions within the cell called organelles.
The eukaryotes are organized into a division of life that is designated as the Eukaryota. The Eukaryota are one of the three branches of living organisms. The other two branches are the Prokaryota and the Archae.
The evolutionary divergence of life into these three groups has been deduced in the pasts several decades. Techniques of molecular analysis have been used, in particular the analysis of the sequence of a component of ribosomal ribonucleic acid (RNA ), which is known as 16S RNA. This RNA species is highly conserved in life forms. Thus, great differences in the sequence of 16 S RNA between a eukaryotic and a prokaryotic microorganism, for example, indicate that the two organisms diverged evolutionarily a very long time ago. A similar 16 S RNA indicates the converse; that evolutionary branching is a relatively recent event.
Eukaryotic cells are about 10 times the size of all but a few prokaryotes. This translates to an internal volume which is very much larger, some 1000 times, that the internal volume of a bacterium. In order to survive, eukaryotes evolved a highly organized internal structure, in order that all the tasks necessary for life can be accomplished in the large internal volume. This internal structure is the fundamental distinguishing aspect of a eukaryote versus a prokaryote.
Functional specialization is the fundamental hallmark of eukaryotes. In larger organisms, such as humans, this specialization gives rise to organs such as the heart, lover, and brain, and to functional organizations such as the immune system . But organization is also evident in microscopic, even single-celled, eukaryotes.
In a eukaryote, the nuclear material is segregated within a specialized region called the nucleus . This feature is a key constituent of eukaryotic cells. Indeed, the word eukaryote means "true nuclei." The nucleus exists because of the presence of the so-called nuclear membrane, which encloses the nuclear material. The nuclear membrane contains pores, through which material can enter and leave the nuclear region. Prokaryotes lack an organized nucleus. Indeed, for many years the presence of a nucleus was the sole key feature that distinguished a eukaryote from a prokaryote.
Most of the eukaryotic DNA (deoxyribonucleic acid ) is present in the nucleus. The remainder is contained within the energy-generating structures known as the mitochondria. The organization of the eukaryotic DNA is very different from bacterial DNA. In the latter, the genetic material is usually dispersed as a large circle throughout the interior of the bacterium, in a gel-like mixture termed the cytoplasm . In contrast, eukaryotic DNA is organized into discrete limb-like structures called chromosomes .
The replication of eukaryotic DNA is also different from that of prokaryotes. The latter is essentially an unwinding of the double helix of DNA, with ongoing complementary copies of daughter DNA strands made from each unwinding parental strand. The result is two double helices. The replication process in eukaryotes is more complex, involving several phases of chromosome replication, segregation to areas of the cell, collection together, and enclosure in a nuclear membrane.
Eukaryotic cells, including microorganisms, contain a specialized functional region known as the endoplasmic reticulum. This network of tubular structures is involved in the manufacture of protein from the template of RNA. In many eukaryotes a region called the Golgi apparatus or Golgi body is associated with the endoplasmic reticulum. The Golgi body is involved with the transport of compounds into and out of the cell.
Another distinctive feature of eukaryotic cells is the aforementioned mitochondria. These are the energy factories of the cell. Additionally, some eukaryotes possess structures called chloroplasts, which use the energy available in light to change carbon dioxide and water into carbohydrates. The carbohydrates provide a ready source of energy for cellular functions. This photosynthetic process is a feature of the microscopic eukaryotes called algae.
Other internal organization of eukaryotes includes lysosomes, which contain enzyme that digest food that is taken into the eukaryote. The lysosome represents a primitive stomach.
Eukaryotic cells such as amoeba possess an internal scaffolding that helps provide the shape and support to the cell. The scaffolding consists of filaments that are made of protein. Depending on the protein the filaments are designated as actin filaments, microtubules, and intermediate filaments.
Eukaryotes such as amoebae and algae are part of a group that is called Protista. More commonly, members of the group are referred to as protists .
The evolutionary branching of eukaryotes from prokaryotes involved the acquisition of regions specialized function within the eukaryotic cell. One of these regions, the mitochondria, was likely derived from the habitation of a eukaryote by a bacterium. Evidence from ultrastructural and molecular studies for a symbiosis between a bacterium and a eukaryote is convincing. Over time, the bacterium became truly a component of the eukaryotic cell. Today, however, the DNA of the mitochondria remains unique, with respect to eukaryotic nuclear DNA.
Likewise, chloroplasts may have had the origin in a symbiotic relationship between a cyanobacterium and a eukaryotic cell. Current evidence does not support the development of any other eukaryotic organelle from a prokaryotic ancestor.
See also Bacterial ultrastructure; Cell cycle and cell division; Mitochondrial DNA