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Do Gametes contain mitochondria/chloroplasts from their parent cell?

Do Gametes contain mitochondria/chloroplasts from their parent cell?



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It has now been established (according to the Cambridge A level text book) that

organisms form a symbiotic partnership, typically by one engulfing the other - a process known as endosymbiosis. Dramatic evolutionary changes result. The classic examples, now confirmed by later work, were the suggestions that mitochondria and chloroplasts were originally free-living bacteria (prokaryotes) which invaded the ancestors of modern eukaryotic cells (cells with nuclei).

It also states that

It was also discovered in the 1960s that mitochondria and chloroplasts contain small, circular DNA molecules, also like those found in bacteria

and lastly

The DNA and ribosomes of mitochondria and chloroplasts are still active and responsible for the coding and synthesis of certain vital proteins, but mitochondria and chloroplasts can no longer live independently.

So my question is:

Is this DNA found in the mitochondria and chloroplasts coded for in the host's (animal's or plant's) DNA.

If not are there fully formed mitochondria and/or chloroplasts in all gametes (obviously chloroplasts only in the plant gametes) which were transferred directly from the parent who had them transferred directly from their parent and so on?

If so are all the mitochondria and chloroplasts of one type identical in a organism? Are they almost identicle in families (of organisms not the classifictaion Family)?


Is this DNA found in the mitochondria and chloroplasts coded for in the host's (animal's or plant's) DNA.

No, the DNA contained in these organelles it not a subset of the nuclear genome. However, part of the original genome of the prokaryote has been moved to nuclear DNA. That is why, as you cited, they "can no longer live independently."

If not are there fully formed mitochondria and/or chloroplasts in all gametes (obviously chloroplasts only in the plant gametes) which were transferred directly from the parent who had them transferred directly from their parent and so on?

As the child organism would eventually need these organelles, and they can only be inherited, at least one of the gamete must contain them.

For the chloroplast, the general rule is that only one of the gamete provides it. For example, in gymnosperm it is the male gamete (pollen), in angiosperm, it is the female gamete (ovule). Either it is just not present in the other gamete, or a specific exclusion mechanism makes it mono-parentally inherited.

Mostly the same for the mitochondria, with the caveat that (motile) spermatozoa contain mitochondria for their metabolic functions (energy to move), but these are discarded when forming the zygote, and only the maternal mitochondria are inherited. (In plants, mostly maternal too with exceptions)

This does mean that there is a lineage of organelle on one of the parent's side, up to the most recent common ancestor (approximately, the first individual of the species). In humans, this translates to a presumed Mitochondrial Eve from which all human mitochondrial DNA descends from.

If so are all the mitochondria and chloroplasts of one type identical in a organism? Are they almost identicle in families (of organisms not the classifictaion Family)?

Every mitochondrion of an individual organism comes from the stock of mitochondria of the zygote, through replication. They are thus very similar, except for cell specialization (giving particular morphology to the organelles), and possible mutations. Same for the chloroplast.

Mitochondria (and chloroplasts) are basic components of the eukaryotic cell, providing essential functions which are highly conserved in a species, let alone related individuals.

However, this does not means the DNA of these organelle is the same for every individual : different sequences may give the same protein, or mutation may affect non-coding segment of the genome. This is the basis for genetic genealogy, retracing family lineage though analysis of DNA, including mitochondrial DNA.


No to your first question. Mitochondrial DNA (m[t]DNA) is individual to the host's DNA- it has it's own DNAs in the organelles itself. The same goes for chloroplasts. The mitochondrial DNA is officially linked to the mother's X-chromosomes, and since the sperm's mitochondria is destroyed and only the maternal egg cell is left, the mother's mtDNA is remained to pass down.

Mitochondria grow, reproduce, and replicate mtDNA by their own - this is another proof that they used to be prokaryotes, not to mention their circular DNA, double-membrance structure, etc…

I am not so sure about the third question of their evolutionary relationships between each other, but you probably have to know that chloroplasts created food by fixing carbon dioxide, while mitochondria broke down sugars to release ATP.


The DNA of Chloroplasts, Mitochondria, and Centrioles

The chapter discusses the evidence for the following conclusions: (1) the cytoplasmic organelles that contain small amounts of deoxyribonucleic acid (DNA) (2) each type of organelle contains its own characteristic DNA (3) the DNA of the organelles is double-stranded and replicates in a semiconservative fashion (4) the DNA codes for specific ribonucleic acids (RNAs) and the RNAs are translated into proteins. Labeling studies with plastids and mitochondria support the hypothesis that DNA codes for molecular ribonucleic acids (mRNA) that is translated to protein. The proteins are required for the growth and differentiation of the proplastid to chloroplast of the pro mitochondrion to mitochondrion and of the procentriole to centriole. Products from the nucleus affect the multiplication and differentiation of the organelles. Concomitanly, products from the organelles affect the nuclear DNA. The multiplicity of plastids and mitochondria in a cell suggests the hypothesis that there may be a number of clones of these bodies in a cell. Thus, the inheritance of an organism may be constituted not only of a nuclear gene pool, but in addition, of gene pools of clones of cytoplasmic organelles. The significance of cytoplasmic genes is discussed in terms of their phenotypic effects and their relation to hybrid vigor, ecology, and cancer.


Introduction

Non-Mendelian inheritance was discovered in plants more than a hundred years ago (Correns 1909 Baur 1909). Subsequent genetic and biochemical analyses revealed uniparental inheritance (UPI) in all eukaryotic lineages investigated. We learned that the basis for UPI is the failure to transmit organellar DNA (orgDNA) to the progeny. Remarkably, however, we have achieved essentially no understanding of why UPI is prevalent.

To address this deficiency, we will first consider the occurrence of UPI among diverse eukaryotes, followed by the properties of the DNA molecules that comprise the chromosomes in the organelles and the nucleus. This information will then be used to evaluate the mechanisms and utility of UPI. My thesis is that UPI is an incidental consequence of cost reduction in the maintenance of orgDNA that is highly susceptible to damage from oxidative stress.


Section Summary

Like a prokaryotic cell, a eukaryotic cell has a plasma membrane, cytoplasm, and ribosomes, but a eukaryotic cell is typically larger than a prokaryotic cell, has a true nucleus (meaning its DNA is surrounded by a membrane), and has other membrane-bound organelles that allow for compartmentalization of functions. The plasma membrane is a phospholipid bilayer embedded with proteins. The nucleolus within the nucleus is the site for ribosome assembly. Ribosomes are found in the cytoplasm or are attached to the cytoplasmic side of the plasma membrane or endoplasmic reticulum. They perform protein synthesis. Mitochondria perform cellular respiration and produce ATP. Peroxisomes break down fatty acids, amino acids, and some toxins. Vesicles and vacuoles are storage and transport compartments. In plant cells, vacuoles also help break down macromolecules.

Animal cells also have a centrosome and lysosomes. The centrosome has two bodies, the centrioles, with an unknown role in cell division. Lysosomes are the digestive organelles of animal cells.

Plant cells have a cell wall, chloroplasts, and a central vacuole. The plant cell wall, whose primary component is cellulose, protects the cell, provides structural support, and gives shape to the cell. Photosynthesis takes place in chloroplasts. The central vacuole expands, enlarging the cell without the need to produce more cytoplasm.

The endomembrane system includes the nuclear envelope, the endoplasmic reticulum, Golgi apparatus, lysosomes, vesicles, as well as the plasma membrane. These cellular components work together to modify, package, tag, and transport membrane lipids and proteins.

The cytoskeleton has three different types of protein elements. Microfilaments provide rigidity and shape to the cell, and facilitate cellular movements. Intermediate filaments bear tension and anchor the nucleus and other organelles in place. Microtubules help the cell resist compression, serve as tracks for motor proteins that move vesicles through the cell, and pull replicated chromosomes to opposite ends of a dividing cell. They are also the structural elements of centrioles, flagella, and cilia.

Animal cells communicate through their extracellular matrices and are connected to each other by tight junctions, desmosomes, and gap junctions. Plant cells are connected and communicate with each other by plasmodesmata.

Additional Self Check Questions

1. What structures does a plant cell have that an animal cell does not have? What structures does an animal cell have that a plant cell does not have?


Cytoplasmic inheritance of mitochondria and chloroplasts in the anisogamous brown alga Mutimo cylindricus (Phaeophyceae)

Based on the morphology of gametes, sexual reproduction in brown algae is usually classified into three types: isogamy, anisogamy, and oogamy. In isogamy, chloroplasts and chloroplast DNA (chlDNA) in the sporophyte cells are inherited biparentally, while mitochondria (or mitochondrial DNA, mtDNA) is inherited maternally. In oogamy, chloroplasts and mitochondria are inherited maternally. However, the patterns of mitochondrial and chloroplast inheritance in anisogamy have not been clarified. Here, we examined derivation of mtDNA and chlDNA in the zygotes through strain-specific PCR analysis using primers based on single nucleotide polymorphism in the anisogamous brown alga Mutimo cylindricus. In 20-day-old sporophytes after fertilization, mtDNA and chlDNA derived from female gametes were detected, thus confirming the maternal inheritance of both organelles. Additionally, the behavior of mitochondria and chloroplasts in the zygotes was analyzed by examining the consecutive serial sections using transmission electron microscopy. Male mitochondria were isolated or compartmentalized by a double-membrane and then completely digested into a multivesicular structure 2 h after fertilization. Meanwhile, male chloroplasts with eyespots were observed even in 4-day-old, seven-celled sporophytes. The final fate of male chloroplasts could not be traced. Organelle DNA copy number was also examined in female and male gametes. The DNA copy number per chloroplast and mitochondria in male gametes was lower compared with female organelles. The degree of difference is bigger in mtDNA. Thus, changes in different morphology and DNA amount indicate that maternal inheritance of mitochondria and chloroplasts in this species may be based on different processes and timing after fertilization.

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Chloroplasts, Genetics of

Abstract

Chloroplasts are the photosynthetic organelles of green algae and plants. Owing to their endosymbiotic origin, they contain their own genome with about 100 genes. Compared with their cyanobacterial ancestors, chloroplasts have lost most of their genes, due to either gene loss or transfer to the nucleus. Therefore, many chloroplast multiprotein complexes are of dual genetic origin with nuclear and chloroplast-encoded subunits. On the DNA level, chloroplast DNA can be subject to homologous recombination and nonhomologous end-joining, the former being exploited in plant biotechnology and the latter in the repair of double-stranded breaks. On the RNA level, some chloroplast sequences undergo editing of RNA, in particular, conversion of C to U. Like mitochondria, chloroplasts can be either inherited from both or only one parent, depending on the size of the gametes and mechanisms that specifically eliminate chloroplast DNA from one parent.


Do Gametes contain mitochondria/chloroplasts from their parent cell? - Biology

The processes in and around mitotic division in eukaryotes are very interesting. The short answer is their organelles do not replicate when the cell does. Some of these organelles have lost their own distinctive cycles however mitochondria (and chloroplasts in plants) have retained some independence. They still have their own DNA.This DNA is one long circular strand much like you would see in a prokaryotic cell. The mitochondrion has its own replication cycle, completely separate from the cell in which it resides. The mitochondria are dispersed throughout the cell so that when the cell divides some mitochondria wind up in one daughter cell and some in the other. This process to the best of our knowledge is not regulated so that a very unlucky cell could actually wind up with no mitochondria at all. (As an aside: This is one of the reasons scientists think that eukaryotic cells evolved from prokaryotic cells.)

Many of the other organelles do divide at the same time as the cell divides (especially organelles that do not have their own DNA). One example is illustrated in the endoplasmic reticulum. This structure divides into many pieces contained in vesicles which are then separated into the two daughter cells. This is a common way for organelles which only have one copy in the cell to segregate into the two daughter cells. These organelles do not appear to replicate before cell division the way DNA does.

During the gap phases (G1 and G2) the cell increases the amount of protein and organelles it contains in preparation for cytokinesis. How exactly the cell partitions its organelles during division is not well understood. It might be a stochastic process or perhaps there is some direction to it (via microtubules. ) It is important to note that some organelles (i.e. mitochondria and chloroplast) have their own DNA and replicate themselves under the control of the cell cycle. Mitochondria divide by binary fission like bacteria.

It seems that detailed information about organelle divisions during mitosis is elusive. I was able to find the following cellbiology

"During the cell division process there is a reorganization of nearly all cell organelles and the cell cytoskeleton.

Interestingly, of the cell organelles, mitochondria appear to undergo there own cycles of division (similar to bacterial division) independent of the cell."

Mitochondrial division is in fact closely associated with cell division and is regulated at "distinct checkpoints" during mitosis, while mitochondrial morphology and segregation is controlled by microtubules in the cell.

A basic college biology textbook, "Life -- The Science of Biology" (Purves, Sadava, Orians, and Heller, 6th edition) states on page 164 "Followingcytokineses, both daughter cells contain all the components of a complete cell. Organelles such as ribosome, mitochondria, and chloroplasts need not be distributed equally between daughter cells as long as some of each are present in both cells accordingly, there is no mechanism with a precision comparable to that of mitosis to provide for their equal allocation to daughter cells."

Another website suggested that organelle division and synthesis occurred primarily during cytokineses cohmetrix

This is not an "edu" website so I can't vouch for its accuracy:

"Cytokineses, the second stage of cell division, begins to occur before mitosisis complete (usually during telophase) and continues after the nuclei of the daughter cells are completely formed. The preliminary steps of cytokineses occur during the growth interphases (called the G phases) of the cell cycle.In the G phases, various membrane structures and organelles, such as the endoplasmic reticulum and Golgi bodies, are produced out of components in the cytoplasm. Therefore, before cytokineses begins, there is growth in the size of the cytoplasm and in the number of its organelles. During the G phases there is also reproduction of the mitochondria and chloroplasts. These organelles contain their own DNA, called organelle DNA, and the organelles' reproduction includes the replication of the organelle DNA.

During cytokineses, the cytoplasm and its contents divide. In animal cells, the cytoplasm divides by pinching inward, whereas in plant cells, a partition, called the cell plate, begins to grow and divide the cytoplasm.Cytokineses is not as precise a process as mitosis because the amount of cytoplasm in a daughter cell will be about half, but not exactly half, the amount of cytoplasm in the parent cell. In addition, each daughter cell will have about half of the organelles from the cytoplasm of the parent cell. In contrast to mitosis, there is no precise mechanism working during cytokinesesto guarantee that each daughter cell receives exactly half of the parent cell's cytoplasm and its organelles.

Cytokineses does not always occur when mitosis occurs because in some cells (such as those found in certain molds) mitosis occurs repeatedly without cytokineses taking place. In this case, each repeated replication of genetic material with no division of cytoplasm (or final separation into new daughter cells) results in cells with two nuclei."


Supporting Information

S1 Fig

Parameters: n = 20, μ = 10 𢄦 , c h = 0.1 and concave fitness (unless indicated otherwise). (A) U 1 replaces B 1 leading to complete uniparental inheritance. (B) Number of generations to reach equilibrium for varying costs of heteroplasmy under concave and convex fitness. U 1 is more advantageous when it takes fewer generations to reach equilibrium. (C) Number of generations to reach equilibrium for varying mutation rates. U 1 replaces B 1 under all tested values of μ. (D) Number of generations to reach equilibrium for different number of mitochondria per cell (as the model with three mitochondrial types is very computationally-intensive, we were unable to examine values of n above 40).

S2 Fig

Parameters: n = 20, μ = 10 𢄧 , c h = 0.2 and concave fitness. (A) Relative advantage of the two genotypes throughout time. The distribution of U 1 B 2 is shown in (B) and B 1 B 2 is shown in (C).

S3 Fig

Parameters: n = 20, μ = 10 𢄧 , c h = 0.2 and concave fitness. (A) Relative advantage of the three alleles throughout time. The distribution of U 1 is shown in (B), B 1 is shown in (C) and B 2 is shown in (D).

S4 Fig

The case in which U 1 mutates into a homoplasmic cell is shown in A-D, while the heteroplasmic case is shown in E-G. We let U 1 mutate in the most heteroplasmic B 1 gamete that had a frequency of > 0.01 at the equilibrium between B 1 and B 2 (which was a gamete with two mutant mitochondria). U 1 gametes appear at generation 0. The heteroplasmic U 1 gametes are quickly lost (first few generations in E and F), leading to much higher levels of U 1 gametes with mutant mitochondria (compare F with B). In turn, this leads to much higher levels of heteroplasmy in B 1 and B 2 (generations 0� in G and H), which results in a steeper drop in w ¯ B 1 and w ¯ B 2 (compare E with A) and a faster production of B 2 gametes that carry mutant mitochondria (about generation 400 in H compared to 1400 in D). Consequently, U 1 replaces B 1 in about half the number of generations when it mutates in a heteroplasmic B 1 gamete compared to a homoplasmic gamete.

S5 Fig

U in is the frequency of U 1 when it mutates from the B 1 gamete. It takes longer for U 1 to replace B 1 when it starts at a lower frequency. Parameters: n = 20, μ = 10 𢄧 , c h = 0.2 and concave fitness.

S6 Fig

Parameters: n = 20, μ = 10 𢄧 and concave fitness. (Note that the y-axis differs by two orders of magnitude between D-F.) Selection against heteroplasmy is strongest in (A) and (D), which leads to very low levels of heteroplasmy in B 1 B 2 cells because few B 2 gametes with mutant mitochondria are produced. Consequently it takes many generations before w ¯ B 1 B 2 starts to drop substantially and U 1 takes longer to replace B 1 as a result. In (B) and (E), selection against heteroplasmy is lower, which leads to more heteroplasmic B 1 B 2 cells and a faster spread of U 1. While the levels of heteroplasmy rise dramatically as selection against heteroplasmy weakens further (C and F), this cannot compensate for the fact that heteroplasmic B 1 B 2 cells are weakly selected against. Thus, U 1 takes longer to replace B 1 compared to B and E.

S7 Fig

U 1 takes increasingly longer to replace B 1 as the number of mitochondria per cell and cost of heteroplasmy increases. Parameters: μ = 10 𢄧 and concave fitness.

S8 Fig

Parameters: n = 20, μ = 10 𢄤 and c h = 0.2. Selection against heteroplasmy is weakest under the concave fitness function, followed by linear and convex fitness respectively (see Fig 1A ). Under concave fitness (A-D), this leads to higher levels of U 1 gametes that carry the mutant haplotype (B). In turn, this leads to more B 2 gametes that carry the mutant haplotype (D) and higher levels of heteroplasmy in B 1 B 2 cells (which can be seen through the high levels of heteroplasmy in the B 1 gametes (C)). Levels of heteroplasmy in the B 1 gamete are lower under linear (E-H) and convex (I-L) fitness functions because these functions select more strongly against heteroplasmic cells. U 1 replaces B 1 in a similar number of generations for each fitness function under these set of parameters because lower levels of heteroplasmy under linear and convex fitness is offset by stronger selection against heteroplasmic B 1 B 2 cells (see Fig 1F ). U 1 spreads at a similar rate for all three fitness functions when c h = 0.2.

S9 Fig

Parameters: s d = s a = 0.1, n = 20, μ = 10 𢄧 and c h = 0.2. In all these cases, the accumulation of mutations is modeled using a concave fitness function. Concave/convex, as noted on the Fig, refers to the fitness function governing selection against heteroplasmy. U 1 replaces B 1 unless both the accumulation of mutations and selection against heteroplasmy are modeled using a concave function (black-solid and red-dashed lines). In these cases, the advantageous and deleterious scenarios converge to the same polymorphic equilibrium with a low level of uniparental inheritance. In the advantageous concave case (black-solid), mutant mitochondria quickly replace wild type mitochondria as the dominant haplotype (this corresponds to the rapid rise in U 1 frequency to about 0.16). B 1×B 2 matings are now less costly because almost all matings involve mutant mitochondria (this stops the rapid spread of U 1). At this point, the advantageous and deleterious scenarios are actually equivalent to each other (mutating from the advantageous mutant to the 'normal' wild type is the same as mutating from the 'normal' wild type to the deleterious mutant since the selection coefficients are the same in both cases). Thus, both cases converge to the same equilibrium. U 1 does not replace B 1 because it is more advantageous for B 1 B 2 cells to have low levels of heteroplasmy (but large numbers of mutant mitochondria) than it is for U 1 B 2 to have a low frequency of cells that are homoplasmic for the wild type haplotype (recall that U 1 B 2 cells quickly segregate into homoplasmic cells thus, mutations from the advantageous mutant to wild type become segregated in homoplasmic wild type cells). This is because the mutant haplotype confers such a large advantage when s a = 0.1. Contrast this with the advantageous case in which selection against heteroplasmy is convex (blue-dotted). Here, too, U 1 stops its rapid spread once the mutant haplotype has replaced the wild type haplotype (U 1 frequency of about 0.35), but now the U 1 slowly spreads until it replaces B 1. Because selection against heteroplasmy is convex in this case, which translates into stronger selection against low levels of heteroplasmy compared to concave selection, it is now less advantageous for B 1 B 2 cells to have low levels of heteroplasmy than it is for U 1 B 2 to have a low frequency of cells that are homoplasmic for the wild type haplotype. As a result, U 1 slowly replaces B 1.

S10 Fig

In A-D, U 1 spreads more quickly when under s a = 0.001. U 1 produces gametes that carry the mutant haplotype, which then rapidly spread in U 1 B 2 cells due to their fitness advantage (compare B to F). Because the mutant haplotype is linked to U 1 (and to B 2 through U 1×B 2 matings), U 1 spreads more rapidly in this scenario. In I-L, U 1 produces much fewer gametes that carry the mutant haplotype (compare J to F) because U 1 B 2 cells that only carry the mutant haplotype are more strongly selected against than U 1 B 2 cells that are homoplasmic for wild type mitochondria. This reduces the number of B 2 gametes with mutant haplotypes (L), which reduces heteroplasmy in B 1 B 2 cells (seen in the lower level of heteroplasmy in B 1 gametes (K)) and slows the spread of U 1.

S11 Fig

(A) P r is below the threshold, which leads to the fixation of the U 1 B 2 genotype. When P r is above the threshold (B-D), the trajectories of the U 1 B 2 and U 2 B 1 genotypes converge. When P r is above the threshold but is much lower than 0.5 (B), the frequency of U 1 B 2 is initially higher than that of U 2 B 1 (because the U 2 gamete initially arises due to recombination between U 1 and B 2 gametes during U 1×B 2 matings). But, because there are initially more U 1 B 2 cells than U 2 B 1 cells, there are more recombination events in U 1 B 2 cells than in U 2 B 1 cells, which drives the U 1:U 2 ratio towards U 2. The frequency of U 2 continues to increase relative to U 1 until P(U 1) = P(U 2), at which point the frequencies of U 1 B 2 and U 2 B 1 converge (B).

S12 Fig

Additional parameters: n = 20, μ = 10 𢄤 , c h = 0.2 and assuming no mating types. Under these conditions, the frequency of uniparental inheritance at equilibrium is 0.118. (A) The relative advantage of the three genotypes. B-D show the relative proportion of the UB (B), BB (C) and UU (D) cells types, where the heteroplasmy category includes all cells with any level of heteroplasmy. E-F show a more detailed distribution of the UB (E), BB (F) and UU (G) cells types at generation 80,000. H-I show the distribution of gamete types for the U (H) and B (I) alleles. The fitness of UU ( w U U ¯ ) drops sharply in the very early stages of the simulation (A) because of an increase in U gametes homoplasmic for mutant mitochondria (H). w UU decreases because U gametes homoplasmic for mutant mitochondria mate with U gametes homoplasmic for wild type mitochondria, which leads to highly heteroplasmic UU cells. Shortly afterwards (up until about 1휐 4 generations), U gametes homoplasmic for mutant mitochondria drop in frequency (H). w UU increases because there are now fewer U×U matings between mutant and wild type gametes. But it never reaches the level of w BB (A) because U gametes homoplasmic for mutant haplotypes remain (compare H to I). Thus, although UU cells have a lower proportion of heteroplasmic cells, these cells have higher levels of heteroplasmy than BB cells (compare F with G recall that cells with low levels of heteroplasmy are weakly selected against when fitness is concave). Because uniparental inheritance is under negative frequency-dependent selection, it does not spread to its maximum level.

S13 Fig

Additional parameters: n = 20, μ = 10 𢄤 , c h = 0.2, convex fitness and assuming no mating types. (A) The relative advantage of the three genotypes. B-D show the relative proportion of the UB (B), BB (C) and UU (D) cells types, where the heteroplasmy category includes all cells with any level of heteroplasmy. E-F show a more detailed distribution of the UB (E), BB (F) and UU (G) cells types at generation 60,000. H-I show the distribution of gamete types for the U (H) and B (I) alleles. Compared to the situation under concave fitness (S12 Fig), when fitness is linear or convex a negligible amount of U gametes are homoplasmic for mutant mitochondria (H). Consequently, there is no noticeable difference between U×U and B×B biparental inheritance matings (compare F to G) and w UU converges with w BB (A). Because U×B matings are more advantageous than the biparental inheritance matings (A), uniparental inheritance spreads to its maximum level under a linear or convex fitness function.

S14 Fig

(A) A three-dimensional fitness function that is similar to the two-dimensional concave function. Low levels of heteroplasmy incur a relatively small fitness cost. (B) A three-dimensional fitness function that is similar to the two-dimensional convex function. Low levels of heteroplasmy incur a relatively large fitness cost.

S1 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S2 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S3 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S4 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S5 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S6 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S7 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S8 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S9 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S10 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium.

S11 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium. Fitness (heteroplasmy) is the fitness function governing the cost of heteroplasmy. The accumulation of deleterious mutations is modeled using a concave fitness function.

S12 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium. Fitness (heteroplasmy) is the fitness function governing the cost of heteroplasmy. The accumulation of deleterious mutations is modeled using a concave fitness function.

S13 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium. Fitness (heteroplasmy) is the fitness function governing the cost of heteroplasmy. Fitness (accumulation) is the fitness function that governs the accumulation of advantageous mutants.

S14 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of the U 1 B 2 genotype at equilibrium. Fitness (heteroplasmy) is the fitness function governing the cost of heteroplasmy. Fitness (accumulation) is the fitness function that governs the accumulation of advantageous mutants.

S15 Table

Values represent the number of generations (휐 3 ) to reach equilibrium for varying values of s a (advantageous selection coefficient) and s d (deleterious selection coefficient). When both haplotypes havel fitness, the population reaches equilibrium in 26(휐 3 ) generations under the same set of parameters. Uniparental inheritance becomes fixed in all cases. Parameters: n = 20, μ = 10 𢄧 , c h = 0.1 and concave fitness.

S16 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of uniparental inheritance at equilibrium (U 1 U 2 for recombination and UU for no mating types). Additional parameters: P r = 0.5 (for recombination).

S17 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of uniparental inheritance at equilibrium (U 1 U 2 for recombination and UU for no mating types). Additional parameters: P r = 0.5 (for recombination).

S18 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of uniparental inheritance at equilibrium (U 1 U 2 for recombination and UU for no mating types). Additional parameters: P r = 0.5 (for recombination).

S19 Table

UPI is maximized at 0.5 when U×U have biparental inheritance (see main text for explanation). UPI frequency (recomb.) is evenly split between the U 1 B 2 and U 2 B 1 genotypes at equilibrium, while the UPI frequency (no mating types) refers to the frequency of the UB genotype at equilibrium. Additional parameters: P r = 0.5 (for recombination).

S20 Table

UPI is maximized at 0.5 when U×U have biparental inheritance (see main text for explanation). UPI frequency (recomb.) is evenly split between the U 1 B 2 and U 2 B 1 genotypes at equilibrium, while the UPI frequency (no mating types) refers to the frequency of the UB genotype at equilibrium. Additional parameters: P r = 0.5 (for recombination).

S21 Table

UPI is maximized at 0.5 when U×U have biparental inheritance (see main text for explanation). UPI frequency (recomb.) is evenly split between the U 1 B 2 and U 2 B 1 genotypes at equilibrium, while the UPI frequency (no mating types) refers to the frequency of the UB genotype at equilibrium. Additional parameters: P r = 0.5 (for recombination).

S22 Table

UPI frequency (recomb.) is given by P(U 1 B 2) + P(U 2 B 1) + P(U 1 U 2)(1 – P b) (at equilibrium), while the UPI frequency (no mating types) is given by P(UB) + P(UU)(1 – P b) (at equilibrium). Additional parameters: P r = 0.5 (for recombination). See S5 Model for how we determined whether or not uniparental inheritance was maximized.

S23 Table

UPI frequency (recomb.) is given by P(U 1 B 2) + P(U 2 B 1) + P(U 1 U 2)(1 – P b) (at equilibrium), while the UPI frequency (no mating types) is given by P(UB) + P(UU)(1 – P b) (at equilibrium). Additional parameters: P r = 0.5 (for recombination). See S5 Model for how we determined whether or not uniparental inheritance was maximized.

S24 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of uniparental inheritance at equilibrium. In rows 7, 8 and 10, in which there are few mitochondria, multiple mitotic divisions, and selection against heteroplasmy after mitosis, U 1 has no selective advantage and does not spread beyond its introductory frequency (when U 1 is introduced at a frequency of 0.01, the frequency of UPI is 0.02). Under these conditions, a mutation for uniparental inheritance could only spread via genetic drift thus, biparental inheritance would be expected to remain stable if it were the ancestral condition. *The simulation in row 5 was stopped after 2 billion generations (before reaching equilibrium) while the spread of UPI was slowed in this simulation, it was not stopped.

S25 Table

In this case, we apply selection after cells have gone through half of their mitotic divisions. After selection, we apply the second half of the mitotic divisions (e.g. in row one: 10 divisions, selection, 10 divisions).

S26 Table

Generations means the number of generations to reach equilibrium. UPI frequency is the frequency of uniparental inheritance at equilibrium. UPI frequency is given by P(U 1 B 2)(1 – P b) (at equilibrium).

S27 Table

We generated pseudo-random parameter values for P b, P U 1 and P U 2 using the 'twister' MATLAB rng. The rng values were normalized so that they sum to 1 because P b + P U 1 + P U 2 = 1 . UPI(U 1) is given by P U 1 ( U 1 U 2 ) + U 1 B 2 , UPI(U 2) is given by P U 2 ( U 1 U 2 ) + U 2 B 1 and BPI is given by P b(U 1 U 2)+B 1 B 2.


Q: What are some advantages of asexual reproduction in plants?

A: The asexual reproduction is the production of new plants without using of seeds, it can incorporate .

Q: Explain how artificial selection is like natural selection

A: Evolution is known as the change or alteration in the features of a species over various different g.

Q: What word is used to describe the release of neurotransmitters to stimulate another cell? .

A: Neurotransmitters are chemicals released from axon terminals when their vesicles fuse releasing the .

Q: If a cell containing 10 chromosomes divides by mitosis, how many daughter cells will be produced? .

A: Cells multiply through cell division in which the new cells are formed from the division of parent c.

Q: Why might a single base-pair mutation in eukaryotic mRNA be less serious than one in prokaryotic mRN.

A: Single base pair mutation in mRNA transcript in Eukaryotes is less serious because mRNA of Eukarotes.

Q: When blood calcium levels are low, PTH stimulates: a. excretion of calcium from the kidneys. b. excr.

A: Answer: Introduction: Blood amounts of calcium are controlled by the parathyroid hormone, that has a.

Q: Tay-Sachs disease is caused by loss of function mutation in a gene on chromosome 15 that codes for a.

A: According to Hardy Weinberg`s equilibrium- p2 + 2pq + q2 = 1 and p + q = 1 p = frequency of the domi.

Q: Explain what the genetic code is and what it is codingfor.

A: Genetic code, the sequence of nucleotides in desoxyribonucleic acid (DNA) and RNA (RNA) that determi.

Q: QUESTION 1 The toe pads of tree frogs are examples of O 1. behavioral traits. 2. structural adaptati.

A: Frogs They belong to the phylum amphibia. Amphibians are the animals that are capable of surviving .


Green algae in the order Charales, and the coleochaetes (microscopic green algae that enclose their spores in sporopollenin), are considered the closest living relatives of embryophytes. The Charales can be traced back 420 million years. They live in a range of fresh water habitats and vary in size from a few millimeters to a meter in length. The representative species is Chara (Figure (PageIndex<2>)), often called muskgrass or skunkweed because of its unpleasant smell. Large cells form the thallus: the main stem of the alga. Branches arising from the nodes are made of smaller cells. Male and female reproductive structures are found on the nodes, and the sperm have flagella. Unlike land plants, Charales do not undergo alternation of generations in their lifecycle. Charales exhibit a number of traits that are significant in their adaptation to land life. They produce the compounds lignin and sporopollenin, and form plasmodesmata that connect the cytoplasm of adjacent cells. The egg, and later, the zygote, form in a protected chamber on the parent plant.

Figure (PageIndex<2>): The representative alga, Chara, is a noxious weed in Florida, where it clogs waterways. (credit: South Florida Information Access, U.S. Geological Survey)

New information from recent, extensive DNA sequence analysis of green algae indicates that the Zygnematales are more closely related to the embryophytes than the Charales. The Zygnematales include the familiar genus Spirogyra. As techniques in DNA analysis improve and new information on comparative genomics arises, the phylogenetic connections between species will change. Clearly, plant biologists have not yet solved the mystery of the origin of land plants.


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