Thursday, January 25, 2018

Cellular Self-Sacrifice

Biology Concepts – apoptosis, synthaesthesia, mitochondria

We often ascribe human traits to objects that do not have thoughts or feelings of their own. This is called anthropomorphism, and it is hard to go through a day without committing this faux pas.

Anthropomorphism is difficult thing to avoid. We are thinking
beings, and we look at other organisms as if we were them –
so we assign our thoughts to them. A typical example would be
the belief that bacteria and viruses MEAN to do us harm, they
have an evil intent when the infect us. It’s just not so……. except
for athlete’s foot fungus. If you have had it before, you know that
it means to make your life miserable.
It is especially difficult to avoid in biology, even scientists will say that an organism “decides” to do this or an enzyme interacts with a substrate “in order to” accomplish that – the enzyme doesn’t have an agenda, it is just chemistry and physics. Assigning feelings or motives to biological entities is often a way to help explain a concept. As long as everyone agrees that it is just a technique, I think it’s fine. The problem arises when not everyone understands that its just a verbal crutch and they start to internalize it.

I can think of one case in particular where individual cells of a multicellular organism seem to be acting with a purpose, even a sense of altruism. It is called apoptosis or programmed cell death. In apoptosis (from Greek meaning, “falling off”) a cell will die “in order to” contribute to the overall health of the organism. It happens all the time. Autumn is full of apoptosis, as this is the mechanism of leaves falling, and is where the original word came from.

You just had about 1 million of your cells die as a result of apoptosis! … There! It just happened again! About a million cells/sec “commit suicide” (there’s some more anthropomorphism) so that you can live. If they didn’t die, you would.

It starts early, when you were in your embryonic stage. Your hands and feet started as single masses, with the bones growing in the appropriate places, at 48 days the skin covering is them all was one unit, more of a mitten than a glove.

In utero, your hands develop with individual fingers, but covered
by tissue all over, then apoptosis divides them into individual
fingers. The same thing happens with your toes…. Unless it doesn’t
work as it should. If it doesn’t, you end up with syndactyly, or fused
Then some of the skin cells between the digits began to die, and your fingers and toes started to become apparent. Sometimes the process doesn’t work completely, and people will have webs between their fingers or toes, or two digits will be fused together completely (syndactyly, syn = same and dactyl = digit). In the normal case, these skin cells are programmed to die. Why have the cell in the first place if it just going to die?

In terms of fetal formation, the cells do serve a purpose when they are formed, but that purpose is only temporary. However, this is not unlike many of your adult cells. The cells dying inside you right now probably had a “job to do,” but now they are worn out and replacements have been made for them. In essence, most of our cells are temporary.

Apoptosis is a group of complex mechanisms that allow cells to die well. We all know about cells that do not die well. If you hit your thumb with a hammer, you kill a few thousand cells. They tear open and dump their cellular contents into the tissue around them. This signals a reaction called inflammation and perhaps a sort of immune response. Inflammation and immune responses are good at cleaning up the damage, but they can cause damage in the process. With a million cells dying every second by apoptosis, you would never survive if every death brought an inflammatory response.

Necrosis is the cell death with inflammation and tissue
destruction. This is what happens in frostbite. Can you
imagine if you had this sort of reaction when undergoing
apoptosis to make your individual fingers in utero?
Dying well means cell death without inflammation. In apoptosis, the mechanisms work to shrink the cell away from its neighbors but keeps the cell membrane intact for most of the time it is dying. This prevents the inflammatory response from being jump started.

Signals from outside the cell can stimulate apoptosis, including hormones, damaging chemicals, or a loss of innervation. Sometimes it can be as little as a cell migrating from where it should be; the lack of the proper neighboring cells triggers the out of place cell to die. These are examples of extrinsic apoptosis.

But the signal could be intrinsic as well. Signals that come from inside the cell could be DNA damage, too many oxygen radicals causing damage to proteins, or even that the cell senses it has been infected by a virus. Viruses turn the cell into a virus factory, then the cell bursts to release the new viral particles and they go on to infect more cells. By initiating programmed cell death, no new viruses are made, so no additional cells will be infected and killed. As Spock would say, "They good of the many outweighs the good of the few, or the one."

The exceptional part about this process is that  the mitochondrion is a crucial instigator in apoptosis. This organelle that is so crucial for life and so important for giving the cell its energy to carry out its functions, is one of the main checkpoints and instruments of programmed cell death.

If the signal for apoptosis comes from within the cell, it results in a change in the membrane of the mitochondrion, with leakage of a protein called cytochrome c out into the cytoplasm. Cytochrome c is usually held within the mitochondrion, so that the apoptosis process is held in check. Once released, this protein complexes with other proteins to form an apoptosome, and this starts a cascade toward death.

If the signal comes from outside the cell, many different receptors and pathways can be involved, but some of these will also affect the mitochondria. There are competing sets of factors in the cytoplasm, some always pushing toward cell death while others apoptosis from proceeding. The delicate balance of the factors that want to disrupt the mitochondrion and those that want to protect it allows the cell to live in harmony with itself until there is a reason to die.

This cartoon is a little detailed, but the take home message
is that many insults can lead to mitochondrial damage
(top arrows) and the damage can lead to several signals
for cell suicide – apotposis (bottom arrows).
The extrinsic signals can cause the balance to shift toward mitochondrial leak of cytochrome c. This leads to apoptosome formation, and this activates caspases and other executioner protein enzymes that will start to destroy the cell from within. Some enzymes cut up the DNA into small pieces so that it is no longer functional. Others force the chromatin and nucleus to condense and shrink (become pyknotic) and stop making ribosomes. Some digest important proteins in the cytoplasm. The sum total of their actions is a non-functional cell, but one that is still intact. Over time, the shrunken and dying cell is recognized by macrophages or other cells that quietly break it up and digest it, all without causing any inflammation.

Apoptosis isn’t just for your looks, as in giving you individual fingers and toes. It plays a role in every system of your body, in other animals, and even in plants. Plant cells undergo a programmed cell death, but it is a little different than animal apoptosis because they also have a cell wall to deal with and they don’t have an immune system to ingest all the dying cells. And the metamorphosis of caterpillars turning into butterflies and tadpoles becoming frogs… that couldn’t happen without a lot of apoptosis.

Your embryonic and juvenile nervous system has millions of neurons it does not need. The connections between some neurons may not be in accordance with how humans process signals, and some dying back of processes and cells is expected (called neural pruning).

Misplaced connections that do not die from apoptosis can lead to some interesting results. Synaesthesia is a group of conditions where sensory input is interpreted in more than one area. For example, if connections between taste and other parts of the brain are not pruned by apoptosis, some people will taste colors, or names will have a certain taste. Many synaesthetes (people with synaesthesia) will see number in their brains as having certain shape or texture. It is believed that most children have near photographic memories and cross innervations among the senses, but that the connections for these abilities die back in order to prevent sensory or memory overload.

It is unfortunate that there aren’t very descriptive pictures
that could show what it is like to have synthaesthesia – sure
you can show a colored word or set  of letters, but you don’t
get the idea of what it is to see it in your head when your
hear a letter or word. This chart shows a little of how the
senses can be combine, each combination has a name, but I like
how Dr. Hugo Heyrman sums it up – Synesthesia is a love story
between the senses.
But this is not the only use of apoptosis in the brain. You have heard the expression, “use it or lose it?” This applies to your brain as well. Neural connections in the brain that are stimulated by experiences or thoughts get reinforced, and are less likely to undergo programmed cell death. Those connections that are not used when young are not kept; it would be a waste of energy.

Your immune system also relies on apoptosis. You have T lymphocytes that are designed to recognize a certain molecule that shouldn’t be in your body. Each population of T cells recognizes a different potential problem guest – millions of them in all. But some of the T cells that are made recognize a particle that looks a lot like one of your own molecules. You don’t want that.

In your thymus and other places in your body, your T cells go through a testing process. If they recognize a protein or molecule that isn’t you, they are allowed to mature and then go out in to the body and patrol for their particular target. But if they are programmed to recognize something that is “self” then they are signaled to undergo apoptosis.

It is a great system and works most of the time, but there are exceptions. Some “non-self” proteins can mimic “self” proteins, and if you start to develop an immune response to them, there may be some cross-reaction with your own cells. Or perhaps some T cells that recognize a “self” protein don’t undergo apoptosis when they should. These issues can result in autoimmune diseases – your immune system is attacking you.

Cancer is a loss of cell cycle control, including the idea that
cells are meant to die at an appropriate time. The problem
is that there are many ways that a cell can circumvent the
apoptosis signals, so you can’t induce apoptosis in all cancer
cells by using just one medicine. Plus, how do you tell the
cancer cells to undergo programmed cell death, 
but tell the normal cells to stay alive?
So - too little apoptosis can be a bad thing. One other big example of this is cancer. Most cells have a life span, they should die at some point. But in some types of cancer, the mutations can tip the balance in the cell and mitochondria toward the survival end; they keep living and dividing and piling up; this is a tumor.

Death is a part of life, and we should be thankful for it.

Novich, S., Cheng, S., & Eagleman, D. (2011). Is synaesthesia one condition or many? A large-scale analysis reveals subgroups Journal of Neuropsychology, 5 (2), 353-371 DOI: 10.1111/j.1748-6653.2011.02015.x

Hänggi, J., Beeli, G., Oechslin, M., & Jäncke, L. (2008). The multiple synaesthete E.S. — Neuroanatomical basis of interval-taste and tone-colour synaesthesia NeuroImage, 43 (2), 192-203 DOI: 10.1016/j.neuroimage.2008.07.018

Eroglu M, & Derry WB (2016). Your neighbours matter - non-autonomous control of apoptosis in development and disease. Cell death and differentiation PMID: 27177021

For more information or classroom activities on apoptosis and synthaesthesia, see:

Apoptosis –

Synaesthesia –

Thursday, January 18, 2018

Biological Fusion Energy

Biology Concepts – mitochondrial dynamics

Stars are the largest fusion reactors around, and organisms do use 
some of the energy our Sun produces by joining two hydrogen atoms
into a helium atom - remember photosynthesis? Fission reactors are 
closer to home, but are much less efficient -- and can melt down
and kill us all.  Cellular fission and fusion are about joining and 
splitting things as well, just without the release of energy.
In the typical picture of a working cell, you would see millions of vacuoles traveling around, joining together and splitting off from organelles. The general proposition is that a bag of stuff fuses (joins) or fissions (separates) from another bag of stuff.

In physics, fission and fusion can be sources of great energy, but in cells they usually require an input of energy. If the processes were the same, we could run the world’s electronics on biology power – a true cell phone!

Fusing and fissioning are easy for vacuoles, they have one membrane. But the mitochondria and chloroplasts we have been looking at for the past few posts have very specific, double membrane structures. The outer membrane and inner membranes form a intermembrane space that is crucial for their function, and the inner membranes have specific forms and structures that are necessary to make carbohydrate or ATP.

Wouldn’t fusing or splitting these organelles destroy the membrane structures needed to maintain their functions? Indeed, the typical cartoon of the cell shows individual mitochondria or chloroplasts floating around in the cell, doing their jobs, but not interacting with the other organelles or with each other.
The structure pictured in green is, believe, it or not, the
mitochondrion of a fibroblast (fibro = fiber and blast =
sprout) cell, one that makes connective tissue. This doesn’t
look much like the mitochondrion in the biology books,
does it? The different strands join together and separate
For mitochondria at least, this picture is misleading. In many cells, the mitochondria do not look like independent structures floating within the cell. They look more like strands of spaghetti on your plate. Mitochondria can also move around, they fuse together and break apart, they are recruited to different subcellular areas based on energy need, and they can exchange organellar content.

All these features (shape, communication, movement, fusion, fission, and exchange) are dynamic, meaning that they change with time and are regulated. First recognized as a regulated process about 10 years ago, this has spawned a new line of research called mitochondrial dynamics.

Changes in morphology are also involved in progression through the cell cycle. A 2009 study showed that in cultured cells, the mitochondria must fuse together into branched networks in order for the cell to enter the phase when it replicates its DNA. Now it appears that this changing mitochondrial morphology is important for other shifts in cell fate. The same group that conducted the 2009 study above showed in May 2012 that mitochondrial fusion and fission are important for oogenesis differentiation (the changes an egg goes through to become different types of cells) in fruit fly egg chambers, implying their importance in differentiation of other cells too.

It appears that fusion and fission help to maintain the correct number of mitochondria, but also work in the preservation of mitochondrial function. Defective proteins can be kicked out if there are normal proteins to replace them. Fusion of mitochondria can provide these normal proteins. In other instances, low oxygen or low carbohydrate concentrations can bring fission and fusion so that the mitochondria can share nutrients and prevent their own degradation.

Most importantly, defective mitochondrial DNA (mtDNA) can be minimized by combining or being replaced it with normal DNA from functioning mitochondria. In most cases, recombination of DNA serves to increase genetic diversity, but with mtDNA it seems the opposite effect is desired. Recombining and exchanging DNA serves to maintain a single uniform genome for all the mitochondria; fusion can preserve the integrity of the mitochondrial genome. Mutations or defects in either exchange, fission, or fusion systems result in poor mitochondrial function and identifiable diseases.

People with Charcot-Marie Tooth have very high
arches, and are most often double jointed. Would
you enjoy having your knees bend the other
direction? I can tell you from personal experience,
that double jointed people are very hard to wrestle
against. They can slip out of whatever hold you try
on them.
If the fusion of mitochondria is defective, a disease called Charcot-Marie-Tooth type 2a may result.  This is a neuronal degenerative disease that usually affects the lower extremities more than the arms. Most cases are caused by defects in the cells that surround the neural axon (the long projection between the cell body and the connection point to other neurons), but in type 2a, the defect is in the axon, specifically the inability of mitochondria to fuse. Therefore, fusion must be important.

In Huntington’s disease, there is too much mitochondrial fission. Huntington’s chorea (chorea = dance, patients with this disease develop large uncontrollable movements that make it look like they are dancing). The cause is an expansion in the huntingtin gene (yes, I spelled it right); a three DNA base repeat (CAG) is mutated and becomes repeated too many times. This affects the function of the huntingtin protein. The age of onset and speed of progression are related to how expanded the triplet repeat is. As of today, this autosomal dominant genetic disease (only need to inherit one mutant gene for it to occur) is untreatable and fatal.

However, the mechanism by which this mutation causes neuron degeneration is just becoming clear.  A 2010 study indicated that the mutant huntingtin protein interacts with the proteins that control mitochondrial fission and makes them overactive. Too much fission disrupts mitochondrial functions and the neurons become defective and then die.

Even more important, in terms of numbers of people affected, is the link between reduced mitochondrial fission and Alzheimer’s disease. Scientists know that it was the build up of amyloid protein that promotes neuron degeneration, but until recently, they didn’t know how it was occurring. It turns out that the plaque proteins can stimulate nitric oxide production, which then damages the fission proteins of the mitochondria.

DRP1 proteins are important for the fission of a
mitochondrion into two mitochondria. They oligomerize
(join together in groups) and pinch the mitochondria
apart. Nitric oxide can damage the DRP1 proteins – so
no mitochondrial fission.

This is huge news because preventing this nitric oxide damage might be a way to slow or stop Alzheimer’s progression. This is a difficult area of research, since nitric oxide is important in many biochemical pathways; just shutting down nitric oxide production everywhere in the body would lead to defective hair growth, blood vessel pressure control, abnormal blood clotting and atherosclerosis, ……oh, and Viagra wouldn’t work either.

The movement of mitochondria within cells is also crucial for their function. The longest cells in your body are your motor neurons. A single cell can be several feet long. Your mitochondria must get to where they are needed along the axon of the neuron, and this requires regulated transport and communication.

Defective transport is one outcome during Charcot-Marie-Tooth type 2a defective mitochondrial fusion and in overstimulation of mitochondrial fission in Huntington’s disease. In addition, defective axonal transport of mitochondria may turn out to be an important early defect in Alzheimer’s disease. In fact, defective transport of mitochondria may play a role in Parkinson’s disease, amyotrophic lateral sclerosis (Lou Gehrig’s disease) and other neurodegenerative diseases that involve defective mitochondrial fusion and fission.

Why might this be….. I’m not sure, but here is a guess. Defective fusion or fission leads to defective function – defective function leads to reduced ATP formation – reduced ATP results in defective energy-requiring functions of the cell, like transport of mitochondria from one place to another. I have no evidence for this, but it is a logical, testable hypothesis. It could be that defective transport is an effect, not a cause, of these diseases -at least in part.

Two of our more famous Parkinson’s patients;
Muhammed Ali and Michael J. Fox. Float like Marty
McFly and sting like a bee?

For Parkinson’s disease, a 2009 study showed that defective mitochondrial transport occurred due to dysfunction in the fusion/fission system, independent of changes in the ATP level. However, ATP production is not the only function of mitochondria. They also work in regulating the amount of calcium in the cell, and altered calcium levels can lead to disruption of the cytoskeletal transport mechanisms. Maybe I need to tweek my hypothesis; it is fusion/fission-mediated defects in several mitochondrial functions that then cause axonal transport changes that are noted in many neurodegenerative disorders. Now design an experiment to test it - this is how scientists go about their work.

So we see that the mitochondria are not static, they are changing all the time and that these changes are crucial for their function and integrity. Here is our exception in the similarities of chloroplasts and mitochondria. It would seem, at least based on current evidence, chloroplasts are relative loners.

This is not to say that can’t be dynamic. We have seen that chloroplasts have a definitive inheritance pattern, either maternal or paternal, and they will fight to maintain this pattern. Chloroplast fusion has been most often described in the zygote (initial cell formed by fusion of the gametes during fertilization, from Greek zygota = joined or yoked together) of algae. In these cases, which are still rare, the chloroplast genome of one of the two fused organelles will be degraded. Fusion of other chloroplasts, as in mature plant cells, either does not occur or has not been studied, because I can’t find any publications describing it.

These are examples of the dynamic activities of chloroplasts.
Stromule connections can be formed between chloroplasts for
the passage of organelle contents. They are usually 0.5 microns
in diameter (1/500,000 of a meter) and can be found in all types
of plastids. Their function – not completely known yet.

On the other hand, chloroplasts aren’t complete loners either. As far back as the 1960’s there were reports saying that chloroplasts might have certain connections at certain times. More recent studies indicate that small connections can be formed between chloroplasts, often called tubular connections or stromules. It is interesting that stromules can be formed between chloroplasts and mitochondria. It is believed that this is one way the plant cell keeps these two organelles close to one another, since their functions, products, and by-products are so interrelated.

You might ask why the mitochondria and chloroplasts that have so much in common differ in their relative dynamic properties. They were both once free organisms that had to have lots of interactions with other members of their species, but only the mitochondria seemed to have preserved it.  Next week, we will look into how this mitochondrial dynamism is even more crucial organism survival – by regulating cell death. Believe it or not, cells have to know how to die well.

Kasturi Mitra, Richa Rikhy, Mary Lilly, and Jennifer Lippincott-Schwartz (2012). DRP1-dependent mitochondrial fission initiates follicle cell differentiation during Drosophila oogenesis J Cell Biol DOI: 10.1083/jcb.201110058

For more information or classroom activities on mitochondrial dynamics or cellular differentiation, see:

Mitochondrial dynamics –

Thursday, January 11, 2018

The Seeds of Inheritance

Biology Concepts – pollen, plastid inheritance, gymnosperms, angiosperms

I am coming to believe that plants are more complex than animals, even more complex than females. Female plants must be the most difficult things on Earth to understand!

Complete flowers have both anthers for pollen and pistils for egg 
fertilization. Incomplete flowers occur on dioecious plants, 
and have either the pistil (gynoecious) or the anther 
(androecious). Dioecious plants cannot self pollinate, unless 
they have both types of incomplete flowers, like coast
redwoods (see last picture).
Yes, there are female plants. In the plant world, species can be monoecious (mono = one, and ecious = household) or dioecious (di = two). Monoecious plants have individuals that produce both male microgametophytes (pollen) and female megagametophytes (oocyctes or ovules). The individual dioecious plants are either androecious (pollen producing) or gynoecious (seed producing). It's okay to ask if a plant is female, but you still shouldn’t ask her age.

This isn’t even the tip of the tip of the iceberg when it comes to diversity in plant reproduction. There are also different ways to produce seeds. The gymnosperms have unenclosed seeds (gymno = naked, and sperm = seed). Gymnosperms include the conifers (cone producers), the cycads that we talked a little about a few weeks ago, and the gnetum plants. Gnetum plants live close to the equator around the globe and include the Ephedra species. It is from these plants that we get ephedrine and pseudoephedrine that work to relieve allergy and cold congestion.

The other type of seed plants is the angiosperms (angio = hidden). These are the flowering plants that have seeds encased in fruits or other structures that help to protect them and to encourage their dispersal.

One way that the gymnosperms and angiosperms differ is in how they inherit their plastid organelles. But even here there is a lot of overlap and exceptions; plants just keep getting more complex.

Gymnosperms have there seeds exposed on the scales
of the cones, while angiosperms have the protected
inside the fruit (except for strawberries).
Angiosperms have a maternal inheritance of chloroplast DNA (cpDNA), much like animals have maternal inheritance of mitochondrial DNA (mtDNA). The reasons for maternal inheritance of cpDNA elude me. For mitochondria, the theory is that damage to the sperm mitochondria would occur during the swim to the oocyte, so it would be smart to ban them from the egg.

But cpDNA is much more passive, they do not have to do a huge amount of work to get to the ovule of the pollinated plant. The pollen tube grows down to the ovule and delivers the sperm cells right to the egg. There must be some other reason, but I don’t know what it might be.

However, there seem to be more exceptions in angiosperm inheritance of cpDNA than there is in animal mtDNA. A few families of plants, like alfalfa (Medicago sativa) and kiwi fruit vine (Actinidia deliciosa), have a strict paternal inheritance of cpDNA.  This is odd since, the angiosperms have a couple of mechanisms for keeping the plastids out of the male gametes.

Every plant species has a distinct pollen shape, which
is why you can be allergic to some plants and not
others. But each pollen grain has the vegetative cell
that becomes the sperms cells and the tube cell. The
tube usually grows from the side that rests on the
fertilized stigma.
The pollen grain contains a few different kinds of cells. There are one or more generative cells; these are the reproductive cells of the pollen. There will also be many non-vegetative cells as well. The generative cell has two nuclei. One will divide to become the two sperm cells, while the other will form the tube cell to deliver the  sperms cells to the ovule.

In many species, when the generative nucleus divides to form sperm, the plastids are partitioned off, and are not included in the sperm cells. This works to ensure maternal inheritance. In other species, the sperm cells may include plastids, but these quickly degenerate and are not delivered to the ovule. Somehow, the alfalfa plants have overcome these mechanisms and even invented a new one to eliminate or exclude the plastids from the ovule, giving strict paternal inheritance.

Going beyond the alfalfa and kiwi fruit ability to preserve their paternal plastids is the fact that a full 20% of angiosperms can show (but don’t have to show), bipaternal inheritance of cpDNA. This is called potential bipaternal plastid inheritance (PBPI) and is controlled by a male gametic trait, called of all things - PBPI trait! Therefore, the fairly strict maternal inheritance of mtDNA in animals (blue mussels excepted) is not matched by cpDNA in angiosperms.

But it gets weirder. The angiosperm exception is normal for the gymnosperm. Gymnosperms tend to have paternal inheritance patterns for cpDNA. This difference is important to note, since scientists often try to use cpDNA inheritance patterns to track seed movements around the world and through evolutionary time, just like human populations are often tracked using mitochondrial ancestry and inheritance.

But this must be frustrating, because there are also exceptions in the paternal inheritance pattern in gymosperms. The Chinese fir (Cunninghamia lanceolata), which isn’t a fir, is native to Asia but was brought to America in the 1800’s. Remember that before molecular biology, most taxonomic classifications were made on just the morphology (shape and look) of an organism, and its grouping and name were based on how it compared to other organisms. Names often get stuck in the language and are hard to change, so many of the misnomers persist.

Godzilla, or Gojira, always seemed surprised when
the other monster grabbed his tail. Here it happens
to be a giant wolfman. Everybody cashed in on the
werewolf brand; I am surprised Abbott and Costello
aren’t in that picture somewhere.
Consider this, we now know that the Japanese pronunciation for the big green movie monster is “go-zeer-a” or “go-jeer-a,” as it was a portmanteau of the Japanese words for gorilla and whale. But when it came to America, it was just assumed that the name was mispronounced in English and that it was supposed to be “god-zill-a.” We know it is wrong, but the wrong name still survives; it's what you get used to that sticks around.

But back to the Chinese fir. This gymnosperm is a conifer that can grown 150 feet tall, but flaunts its individuality by having a maternal inheritance pattern for cpDNA – much more angiosperm-like behavior than gymnosperm. And this is even odder because the Chinese fir is an older gymnosperm, a much more distant relative to the angiosperms than many gymnosperms that have a strict paternal cpDNA inheritance.

Gymnosperms that show maternal cpDNA inheritance are rare, or just less studied, so one might assume that paternal cpDNA inheritance is fairly strict – wrong. Many gymnosperms have bipaternal inheritance patterns of plastids, so the mechanism might be different from angiosperms, but is no more consistent than that of the flowering plants.

Finally, there is the issue of crossbreeding. In this animal mtDNA and plant cpDNA seem to be similar. Whatever the dominant form of inheritance is seen in natural breedings, the numbers get screwed up when cross breeding occurs. We saw that paternal inheritance of mtDNA in mice was much likely in the mating of different species (interspecific breeding).

The passionflower vine can grow to be 10 meters high
and is the source of the passion fruit that I enjoy so
much. The fruit protects the fertilized seeds that
probably have paternal cpDNA, since most of the
varieties we eat are hybrids of different species.
In plants, this also holds, and may even be more discrepant. Take the passion flowers  (family Passiflora) for instance. Intraspecific breeding (same species) showed the maternal cpDNA inheritance one might expect. But in interspecific crosses the inheritance was 100% paternal. This must represent some attempt to limit the genetic diversity of the organellar genomes, but I leave it to you to explain the reason for it.

The similarity between mitochondrial and plastid inheritance in hybrids brings up another issue – what about mitochondrial inheritance patterns in plants?

It turns out that most plants that have been studied for mtDNA inheritance have a maternal inheritance pattern, just like animals. Amazingly, this includes the gymnosperms, most of which have paternal inheritance of cpDNA. But even some plants with maternal cpDNA patterns can pass on paternal mitochondria. An example of this is the banana - tomorrow morning you can feel like a rebel for garnishing your cornflakes with such an outlaw fruit.

However, the reason would be different. Remember that sperm have their mitochondria in their tails, and in most animals, this is not included in what enters the egg or is degraded just after entering. But few plants have flagellar sperm (like the cycads we talked about before). The sperm mtDNA is not exposed to anymore oxygen radical damage than the ovule mtDNA, yet there is most often uniparental, maternal inheritance.

Coastal redwoods can reach up to 110 meters
(360 ft) tall, but their roots may only go 6 ft.
underground. What's holding this tree in place?
It has two different types of leaves, and has male
and female branches and flowers, but all its
mitochondria and chloroplasts come from one
place, its father.
The interesting cases are those like the gymnosperms; paternal cpDNA, but maternal mtDNA. Once again, the plants are much more complex and intricate in their behaviors than animals, as two separate mechanisms for organellar retention and degradation must be at work in these plants. But even here there can be exceptions. The coast redwood (Sequoia sempervirens) has normal gymnosperm (paternal) inheritance of cpDNA, but it also has paternal inheritance of mtDNA! And the Chinese fir, which breaks the rules and is a gymnosperm with maternal inheritance of cpDNA, also makes itself exceptional in that it has paternal inheritance of mtDNA! Very confusing.

So mitochondria and chloroplasts both work in energy production, both evolved through endosymbiosis, both have single, circular chromosomes (with exceptions), and both have uniparental inheritance patterns (with exceptions). Next week, let’s look a behavior that is different in these two organelles.

Zhang Q, & Sodmergen (2010). Why does biparental plastid inheritance revive in angiosperms? Journal of plant research, 123 (2), 201-6 PMID: 20052516

Bendich AJ (2013). DNA abandonment and the mechanisms of uniparental inheritance of mitochondria and chloroplasts. Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology, 21 (3), 287-96 PMID: 23681660

For more information or classroom activities on monoecious/dioecious plants, angiosperms, gymnosperms, or plastid inheritance, see:

Monoecious/dioecious –

Angiosperms –

Gymnosperms –

Plastid inheritance -