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Self-incompatibility

From Wikipedia, the free encyclopedia

Self-incompatibility (SI) is a general name for several genetic mechanisms in angiosperms, which prevent self-fertilization and thus encourage outcrossing and allogamy. It should not be confused with genetically controlled physical or temporal mechanisms that prevent self-pollination, such as heterostyly and sequential hermaphroditism (dichogamy).

In plants with SI, when a pollen grain produced in a plant reaches a stigma of the same plant or another plant with a similar genotype, the process of pollen germination, pollen-tube growth, ovule fertilization and embryo development is halted at one of its stages and consequently no seeds are produced. SI is one of the most important means of preventing inbreeding and promoting the generation of new genotypes in plants, and it is considered as one of the causes for the spread and success of angiosperms on the earth.

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Crash Course Philosophy is brought to you by Squarespace. Squarespace: share your passion with the world. Let’s say, for the sake of argument, that you love your father. By which I mean, you want him to be alive. And let’s also assume that you don’t have any attachments to your mother that you might describe as... romantic. Well, guess who thought felt the same way about his parents? Oedipus. According to ancient Greek legend, when Oedipus was born, a prophecy foretold that he would kill his father and marry his mother. So his father left baby Oedipus in the wilderness, assuming he would die, and the prophecy would then not come true. But instead, the abandoned baby was discovered and raised by another family. As an adult, Oedipus learned of the prophecy that he would kill his father and marry his mother. So, not knowing he was adopted, he left his adoptive parents in order to avoid fulfilling that prophecy, figuring that if he wasn’t near them, it couldn’t come true. Lo and behold, as he was trying to flee his fate, Oedipus killed a stranger in a fit of rage, who turned out to be the father he had never met. He then proceeded to marry the dead man’s widow, who was actually his mother, though he didn’t know it. Needless to say, this is a fate that, needless to say, any of us would like to avoid. But for philosophers, the whole point of the story of Oedipus is: there is no escaping fate. [Theme Music] Are we free? I mean, on the one hand, most of us have the clear sense that we are. We feel free. We feel like we make all sorts of decisions that lead to both beliefs and actions that are wholly of our own choosing. Like, I could do that. I had oatmeal this morning because I felt like it. This view – that humans are capable of entirely free actions – is known as libertarian free will. And to be clear, libertarian free will is nothing like political libertarianism. Both views get their name from the word liberty, but political libertarians are all about freedom from government intervention, while people who accept libertarian free will could be anything from political libertarians to socialists. They just think that, metaphysically, we can act freely. So a lot of us figure that our thoughts and actions are free. But, most of us also believe that every effect has a cause, And that everything that happens now, in the present, is the necessary result of events that occurred in the past. This view is known as hard determinism. And many of the people watching this probably think that they believe in both things; that many of your actions are free, and that the world is governed by cause and effect. But, it turns out, you can’t rationally hold both views. Because, traditionally, libertarians have defined free actions according to what’s known as the Principle of Alternate Possibilities. That might sound like the plot device for a sci-fi show, but this principle says that an action is free only if the agent – that is, the person doing the thing – could have done otherwise. So, truly free actions require options. Determinism, by contrast, doesn’t allow options. It holds that every event is caused by a previous event. Which means that an agent can never have done anything other than what they did, and therefore, they are never free. But let’s look at these two options more closely. And also, let’s look at my breakfast. Libertarianism says that my decision to eat oatmeal this morning wasn’t necessarily caused by anything that happened before it. Instead, it could have been the result of non-physical events – specifically, my own thoughts – that originated right at that point. I ate oatmeal because I decided to eat oatmeal! End of story. But libertarianism runs counter to what we know about the workings of the physical world, with one thing causing another. So libertarians need a way to account for their view. One way they do that is by making a distinction between what’s known as event causation, and agent causation. Event causation means that no physical event can occur without having been caused by a previous physical event. So, many libertarians concede that the physical world itself is deterministic. Like, a baseball is flying through the air because someone hit that ball with a bat. But many libertarians also argue that there’s such a thing as agent causation, which says that an agent – a being propelled by a mind – can start a whole chain of causality that wasn’t caused by anything else. So, the person who hit the ball most likely did so because they just decided to do it. By this logic, agents have the ability to affect the causal chain of the universe. They can make stuff happen on their own. But, many philosophers find this idea untenable. Where would these free decisions, the ones that launch entirely new causal chains, come from, they ask? Are they simply random? What would compel an agent to make one decision, and not another? And if you can answer those questions – if you can explain what would cause an agent to act – Then well, you’ve just reinforced the position that actions are caused, rather than free. The fact is, it’s pretty difficult to find arguments that support libertarian free will. The best argument in favor of it seems to be that it just feels an awful lot like we’re free. And libertarians argue that we shouldn’t discount the legitimacy of our own personal, subjective experiences – so if we feel so free, we should seriously consider the possibility that we are. That point has a certain intuitive appeal. But if you can’t come up with an argument to defend your feeling, then good philosophical reasoning recommends that you reject it, or at least withhold judgment until you can get some evidence together. So now let’s see if the hard determinists can do any better. 18th century French philosopher Baron D’Holbach said that none of our actions are actually free. D’Holbach believed that everything that’s happening right now is the result of an unbroken chain of events. Everything, he said, is the inevitable result of what came before. Including everything that we do! Our actions are caused in the same way that, say, home runs are caused by bats hitting balls, or tornadoes are caused by warm air systems hitting cool air systems in the right conditions. This means that humans and our actions are just part of the physical world, bound by its physical laws. This belief is often explained through a view known as reductionism. Reductionism is the view that all parts of the world, and of our own experience, can be traced back – or reduced down – to one singular thing. So, for example, you see your mind as being capable of making free decisions. You think that what goes on in your head when you make a choice is not at all like bats and balls. But, well, mental states are brain states, or at least they’re tied directly to your brain. And brain states are biological. And biological states are physical states. And the physical world – as we already said – is deterministic. There’s just no room for free will in this picture. We think we’re free - but we’re not. And really, as scientific thinkers, why would we assume that we are? Why would we think that we’re any different than everything else in the universe? What would make us so special? Libertarians are right that it’s really hard to disregard the feeling of freedom. If I didn’t choose to eat oatmeal this morning, why do I feel like I did? And what made me do it? But hard determinists say that the difference between the causes of human actions and the causes of physical events – like a bat hitting a ball – is that our actions have all sorts of invisible causes that happen in our brains. Specifically, when beliefs team up with our desires and our temperament, they say, you get a deliberate human action. Combine my belief that oatmeal is nutritious, with my desire for healthy nourishment, and the temperament that predisposes me to enjoy warm, carby comfort foods, and ta-da! – you get oatmealy breakfast! Now, you might argue that those particular beliefs, desires, and temperaments might lead to any number of breakfast choices – cream of wheat, maybe, or some granola. But, if you dig deep enough, you’d see that there are factors that rule out those options – as well as every other option. Maybe I’m a little worried about one of my fillings coming loose, so I’m shying away from the granola because it’s too crunchy. Or I just don’t think about cream of wheat very often. I mean, they don’t have very good brand awareness anymore. What even is cream of wheat exactly? And the oatmeal is sitting right there in front of me. Or maybe I think briefly of making one of those quinoa breakfast bowls that are so hip right now. But my lazy temperament, or my belief that I’m running late, pushes me to choose the 90-seconds-in-the-microwave option. See how it works? All you have to do is change one factor – a belief, desire, or temperament – and you’ll get a different outcome. Hard determinists argue that, just because we can’t pinpoint the exact factors that led us to an action, we could, in theory isolate them – if we knew enough about all the beliefs, desires, and temperaments swirling around in our brains. So, in this view, what we call “decisions” are really just the inevitable results of a bunch of mental stuff combining in just the right way. And maybe it feels free. But it’s not. But hold up! Isn’t there some way out of this? Like, what if I have someone choose my breakfast for me? Or what if I fall back on randomness, by, like, flipping a coin? After all, if I just flipped a coin, then it wouldn’t look like that decision was made by beliefs, desires, and temperaments. But, well, no such luck. Because even if I thought I chose randomly, my decision to flip the coin, or who I asked to pick for me, was just as determined as everything else. And guess what! If you’re getting angry right now about me telling you none of your choices are free, well, that anger was determined! If you’re finding this whole topic confusing, or boring yep – still determined. You think you can just freely choose to stop playing this video, but if you’re still watching me, good news: that’s determined too! Determinists believe that you can’t help but feel and react the way you’re reacting right now. You can think you’re choosing to act in ways that conform to the character that you’ve selected and shaped for yourself, but even that “choice” is the result of all sorts of already-determined factors about you and your place in the world. Hard determinism is tough to refute. And it has some really uncomfortable implications. It means the deeply held feeling most of us have that we actually make free decisions? Is just wrong. And the whole concept of personal responsibility is thrown out the window, too. As D’Holbach put it, we’re all just “cogs in a machine,” doing what we were always meant to do, with no actual volition. Oedipus had to kill his dad and marry his mom. I had to eat the oatmeal. And you? You just had to keep watching! You couldn’t turn away! Today we learned about libertarian free will and it’s counterpoint, hard determinism. Next time, we’ll see if some middle ground can be found between determinism and libertarianism. And I sure hope there can be. Today's episode of Crash Course Philosophy was inevitably made possible by Squarespace. Squarespace is a way to create a website, blog or online store for you and your ideas. Squarespace features a user-friendly interface, custom templates and 24/7 customer support. Try Squarespace at squarespace.com/crashcourse for a special offer. Squarespace: share your passion with the world. Crash Course Philosophy is produced in association with PBS Digital Studios. You can head over to their channel and check out a playlist of the latest episodes from shows like Coma Niddy, Deep Look, and First Person. This episode of Crash Course was filmed in the Doctor Cheryl C. Kinney Crash Course Studio with the help of these awesome people and our equally fantastic graphics team is Thought Cafe.

Contents

Mechanisms of single-locus self-incompatibility

The best studied mechanisms of SI act by inhibiting the germination of pollen on stigmas, or the elongation of the pollen tube in the styles. These mechanisms are based on protein-protein interactions, and the best-understood mechanisms are controlled by a single locus termed S, which has many different alleles in the species population. Despite their similar morphological and genetic manifestations, these mechanisms have evolved independently, and are based on different cellular components;[1] therefore, each mechanism has its own, unique S-genes.

The S-locus contains two basic protein coding regions - one expressed in the pistil, and the other in the anther and/or pollen (referred to as the female and male determinants, respectively). Because of their physical proximity, these are genetically linked, and are inherited as a unit. The units are called S-haplotypes. The translation products of the two regions of the S-locus are two proteins which, by interacting with one another, lead to the arrest of pollen germination and/or pollen tube elongation, and thereby generate an SI response, preventing fertilization. However, when a female determinant interacts with a male determinant of a different haplotype, no SI is created, and fertilization ensues. This is a simplistic description of the general mechanism of SI, which is more complicated, and in some species the S-haplotype contains more than two protein coding regions.

Following is a detailed description of the different known mechanisms of SI in plants.

Gametophytic self-incompatibility (GSI)

In gametophytic self-incompatibility (GSI), the SI phenotype of the pollen is determined by its own gametophytic haploid genotype. This is the more common type of SI.[2] Two different mechanisms of GSI have been described in detail at the molecular level, and their description follows.

The RNase mechanism

The female component of GSI in the Solanaceae was found in 1989.[3] Proteins in the same family were subsequently discovered in the Rosaceae and Plantaginaceae. Despite some early doubts about the common ancestry of GSI in these distantly related families, phylogenetic studies[4] and the finding of shared male determinants (F-box proteins)[5][6][7][8] clearly established homology. Consequently, this mechanism arose approximately 90 million years ago, and is the inferred ancestral state for approximately 50% of all plants.[4][9]

In this mechanism, pollen tube elongation is halted when it has proceeded approximately one third of the way through the style.[10] The female component ribonuclease, termed S-RNase[3] probably causes degradation of the ribosomal RNA (rRNA) inside the pollen tube, in the case of identical male and female S alleles, and consequently pollen tube elongation is arrested, and the pollen grain dies.[10]

The male component was only recently putatively identified as a member of the "F-box" protein family.[8] Despite some fairly convincing evidence that it may be the male component, several features also make it an unlikely candidate.

The S-glycoprotein mechanism

The following mechanism was described in detail in Papaver rhoeas. In this mechanism, pollen growth is inhibited within minutes of its placement on the stigma.[10]

The female determinant is a small, extracellular molecule, expressed in the stigma; the identity of the male determinant remains elusive, but it is probably some cell membrane receptor.[10] The interaction between male and female determinants transmits a cellular signal into the pollen tube, resulting in strong influx of calcium cations; this interferes with the intracellular concentration gradient of calcium ions which exists inside the pollen tube, essential for its elongation.[11][12][13] The influx of calcium ions arrests tube elongation within 1–2 minutes. At this stage, pollen inhibition is still reversible, and elongation can be resumed by applying certain manipulations, resulting in ovule fertilization.[10]

Subsequently, the cytosolic protein p26, a pyrophosphatase, is inhibited by phosphorylation,[14] possibly resulting in arrest of synthesis of molecular building blocks, required for tube elongation. There is depolymerization and reorganization of actin filaments, within the pollen cytoskeleton.[15][16] Within 10 minutes from the placement on the stigma, the pollen is committed to a process which ends in its death. At 3–4 hours past pollination, fragmentation of pollen DNA begins,[17] and finally (at 10–14 hours), the cell dies apoptotically.[10][18]

Sporophytic self-incompatibility (SSI)

In sporophytic self-incompatibility (SSI), the SI phenotype of the pollen is determined by the diploid genotype of the anther (the sporophyte) in which it was created. This form of SI was identified in the families: Brassicaceae, Asteraceae, Convolvulaceae, Betulaceae, Caryophyllaceae, Sterculiaceae and Polemoniaceae.[19] Up to this day, only one mechanism of SSI has been described in detail at the molecular level, in Brassica (Brassicaceae).

Since SSI is determined by a diploid genotype, the pollen and pistil each express the translation products of two different alleles, i.e. two male and two female determinants. Dominance relationships often exist between pairs of alleles, resulting in complicated patterns of compatibility/self-incompatibility. These dominance relationships also allow the generation of individuals homozygous for a recessive S allele.[20]

Compared to a population in which all S alleles are co-dominant, the presence of dominance relationships in the population, raises the chances of compatible mating between individuals.[20] The frequency ratio between recessive and dominant S alleles, reflects a dynamic balance between reproduction assurance (favoured by recessive alleles) and avoidance of selfing (favoured by dominant alleles).[21]

The SI mechanism in Brassica

As previously mentioned, the SI phenotype of the pollen is determined by the diploid genotype of the anther. In Brassica, the pollen coat, derived from the anther's tapetum tissue, carries the translation products of the two S alleles. These are small, cysteine-rich proteins. The male determinant is termed SCR or SP11, and is expressed in the anther tapetum as well as in the microspore and pollen (i.e. sporophytically).[22][23] There are possibly up to 100 polymorphs of the S-haplotype in Brassica, and within these there is a dominance hierarchy.

The female determinant of the SI response in Brassica, is a transmembrane protein termed SRK, which has an intracellular kinase domain, and a variable extracellular domain.[24][25] SRK is expressed in the stigma, and probably functions as a receptor for the SCR/SP11 protein in the pollen coat. Another stigmatic protein, termed SLG, is highly similar in sequence to the SRK protein, and seems to function as a co-receptor for the male determinant, amplifying the SI response.[26]

The interaction between the SRK and SCR/SP11 proteins results in autophosphorylation of the intracellular kinase domain of SRK,[27][28] and a signal is transmitted into the papilla cell of the stigma. Another protein essential for the SI response is MLPK, a serine-threonine kinase, which is anchored to the plasma membrane from its intracellular side.[29] The downstream cellular and molecular events, leading eventually to pollen inhibition, are poorly described.

Other mechanisms of self-incompatibility

These mechanisms have received only limited attention in scientific research. Therefore, they are still poorly understood.

2-locus gametophytic self-incompatibility

The grass subfamily Pooideae, and perhaps all of the family Poaceae, have a gametophytic self-incompatibility system that involves two unlinked loci referred to as S and Z.[30] If the alleles expressed at these two loci in the pollen grain both match the corresponding alleles in the pistil, the pollen grain will be recognized as incompatible.[30]

Heteromorphic self-incompatibility

A distinct SI mechanism exists in heterostylous flowers, termed heteromorphic self-incompatibility. This mechanism is probably not evolutionarily related to the more familiar mechanisms, which are differentially defined as homomorphic self-incompatibility.[31]

Almost all heterostylous taxa feature SI to some extent. The loci responsible for SI in heterostylous flowers, are strongly linked to the loci responsible for flower polymorphism, and these traits are inherited together. Distyly is determined by a single locus, which has two alleles; tristyly is determined by two loci, each with two alleles. Heteromorphic SI is sporophytic, i.e. both alleles in the male plant, determine the SI response in the pollen. SI loci always contain only two alleles in the population, one of which is dominant over the other, in both pollen and pistil. Variance in SI alleles parallels the variance in flower morphs, thus pollen from one morph can fertilize only pistils from the other morph. In tristylous flowers, each flower contains two types of stamens; each stamen produces pollen capable of fertilizing only one flower morph, out of the three existing morphs.[31]

A population of a distylous plant contains only two SI genotypes: ss and Ss. Fertilization is possible only between genotypes; each genotype cannot fertilize itself.[31] This restriction maintains a 1:1 ratio between the two genotypes in the population; genotypes are usually randomly scattered in space.[32][33] Tristylous plants contain, in addition to the S locus, the M locus, also with two alleles.[31] The number of possible genotypes is greater here, but a 1:1 ratio exists between individuals of each SI type.[34]

Cryptic self-incompatibility (CSI)

Cryptic self-incompatibility (CSI) exists in a limited number of taxa (for example, there is evidence for CSI in Silene vulgaris, Caryophyllaceae[35]). In this mechanism, the simultaneous presence of cross and self pollen on the same stigma, results in higher seed set from cross pollen, relative to self pollen.[36] However, as opposed to 'complete' or 'absolute' SI, in CSI, self-pollination without the presence of competing cross pollen, results in successive fertilization and seed set;[36] in this way, reproduction is assured, even in the absence of cross-pollination. CSI acts, at least in some species, at the stage of pollen tube elongation, and leads to faster elongation of cross pollen tubes, relative to self pollen tubes. The cellular and molecular mechanisms of CSI have not been described.

The strength of a CSI response can be defined, as the ratio of crossed to selfed ovules, formed when equal amounts of cross and self pollen, are placed upon the stigma; in the taxa described up to this day, this ratio ranges between 3.2 and 11.5.[37]

Late-acting self-incompatibility (LSI)

Late-acting self-incompatibility (LSI) is also termed ovarian self-incompatibility (OSI). In this mechanism, self pollen germinates and reaches the ovules, but no fruit is set.[38][39] LSI can be pre-zygotic (e.g. deterioration of the embryo sac prior to pollen tube entry, as in Narcissus triandrus[40]) or post-zygotic (malformation of the zygote or embryo, as in certain species of Asclepias and in Spathodea campanulata[41][42][43][44]).

The existence of the LSI mechanism among different taxa and in general, is subject for scientific debate. Criticizers claim, that absence of fruit set is due to genetic defects (homozygosity for lethal recessive alleles), which are the direct result of self-fertilization (inbreeding depression).[45][46][47] Supporters, on the other hand, argue for the existence of several basic criteria, which differentiate certain cases of LSI from the inbreeding depression phenomenon.[38][43]

Self-compatibility (SC)

Approximately one half of angiosperm species are SI,[48] the remainder being self-compatible (SC). Mutations that break down SI (resulting in SC) may become common or entirely dominate in natural populations. Pollinator decline, variability in pollinator service, the so-called "automatic advantage" of self-fertilisation, among other factors, may favor the loss of SI. Similarly, human-mediated artificial selection through selective breeding may be responsible for the commonly observed SC in cultivated plants. SC enables more efficient breeding techniques to be employed for crop improvement.

See also

References

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