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 -

Thursday, January 4, 2018

Every Day Should Be Mother’s Day

Biology concepts – inheritance patterns, mitochondria, fertilization, lineage, mitochondrial Eve

What do the “The Battle Hymn of the Republic”, Mother’s Day, and all your mitochondria all have in common?

Julia Ward Howe wrote the words for The
Battle Hymn of the Republic after meeting
Abraham Lincoln. She wrote it as a poem,
but also as new lyrics for the existing song
called, John Brown’s Body. I wonder if she
had copyright issues to deal with.
The first two are easy; Julia Ward Howe wrote the Battle Hymn of the Republic as a Union anthem during the Civil War, but just 12 years later proposed a national day of mourning and protest for mother’s of sons who killed sons of other mother’s. She had come to regret her support of the Civil War and wanted July 4th to be converted into a protest day by mother’s to ban future wars.

This didn’t go over that well, but the daughter of one of her followers, Julia M. Jarvis, re-purposed the proclamation to celebrate her own mother’s dedication to church and community. This caught on, and in 1912 Jarvis’ home state of West Virginia officially recognized Mother’s Day. Two years later, President Woodrow Wilson declared that the second Sunday in May should be a national observance of a Mother’s Day.

But what has it got to do with your mitochondria? Well, you owe your mom a debt of gratitude for every one of your mitochondria. All of yours came from hers – Dad played no role in your cellular ATP factories.

Here's how it works. Your somatic cells (all your cells except the eggs or sperm) have two copies of each chromosome, but we know that your chromosomes aren’t the only DNA in your cells. Your mitochondria have their own chromosome; it’s circular like the prokaryotic ancestor it came from during endosymbiosis. How do you inherit that DNA?

In this electron micrograph of the sperm you
can see the dark nucleus which houses the
chromosomal DNA. Above the acrosome, or
head, you can see the mitochondria packed
into around the tail proteins. Their ATP is
used to whip the tail for locomotion.
The egg has loads of mitochondria, about a million in each oocyte (egg cell). On the other hand, each sperm has only about 100. This makes sense, the body must produce billions of sperm, but only a few eggs, so it has to ration the mitochondria to all those sperm cells.

The important issue is where the mitochondria are located. The oocyte mitochondria are inside the egg, waiting for a single sperm to enter and begin the process of making a new human (for example). All the mitochondria of the sperm are located in the first part of the tail, called the midpiece or mitochondrial sheath. This also makes sense, as it is the tail’s movement that propels the sperm toward the egg, All of this tail wagging requires a great amount of ATP.

The sperm meets the egg and fuses with the oocyte membrane, but not all of it enters the egg cell. Only the head, or acrosome makes entrance; it has the haploid chromosomal DNA that is your father’s contribution to your genetic makeup. The sperm midpiece, will all its mitochondria remain on the outside of the egg and does not contribute to you being you.

That is how it came to be that you got all your mitochondria from your mother! We all did. The process is called maternal inheritance of mtDNA, and it is has implications for tracking the history of human life.

A journal cover for the issue dedicated to DNA
repair enzymes. Who says scientists don’t have
a sense of humor? Actually, this may just have been
how one guy showed up to the lab that day; his
mind was on science, not fashion.

Mitochondrial DNA doesn’t change much over time, but it does change. Every time your DNA replicates, mistakes are made. “To err is mammalian,” and your DNA polymerase (polymer = long chain, and ase = enzyme that makes) is mammalian. Consider that the DNA polymerase is adding nucleotides to a growing chain at a rate of about 1000/second – some mistakes are bound to occur.

Most of these mistakes are caught and fixed by a series of proofreading and mismatch repair functions, but some mistakes get through. These random mutations often have no effect on the function of the gene product, but if they aren’t fixed, they become permanent and are passed on the next time the DNA is replicated.

Over time, the changes add up. The 50th generation mtDNA necessarily looks different from the 1st generation DNA. Mutations that hurt the function could very well prevent reproductive success (the ability to mate and produce viable offspring), so the changes that we see over time usually are the ones that have little effect on function.

This random mutation wouldn’t matter much if you got half your mitochondria from Pop and half from Mom, there would be random passing on of mitochondrial DNA and probably some recombination, so  the 50th generation wouldn’t look much at all like the first. But you get all of your mitochondria from Ma, and she got hers from her ma, and she got hers from her ma, ….. so that there is a straight line back in your family history.
The rate of mutation and the pattern of mutation
in the mtDNA can not only help us date mtEve, but
can help track the migration of humans out of Africa
and around the world. The numbers with a k =
thousands of years ago.
The maternal inheritance of mtDNA allows scientists to trace family lineage through molecular biology (to balance the sexes, you can trace paternal lineage through the Y sex chromosome as well). In fact, with a large enough sample size, you could literally see that all humans are related! Trace the changes in mtDNA backwards far enough and they will all converge on a single female; the mother of all mothers - “Mitochondrial Eve.” This isn’t the same as a Biblical Eve – just the last female to whom we are all related. We don’t know who mtEve was, where mtEve was, or when mtEve was because we don’t have enough samples from enough generations.

The most current estimate is that mtEve lived about 200,000 years ago, although the timing is just that, an estimate. The sampling and math are dependent on knowing the rate of mutation of the hypervariable regions (part of the mtDNA that mutates faster than the other parts) and knowing that this rate has been constant and predictable. Does that sound like the biology you know? The assumption doesn’t invalidate the idea of mtEve, it just makes sending her birthday card difficult.

Even if we don’t know who Eve was, we can talk about her “daughters.” These are the unnamed females to whom we can trace back large numbers of living and deceased humans. Geneticist Bryan Sykes wrote a book called The Seven Daughters of Eve in 2001, but we now consider that we have really defined about 10-12 daughters. With twelve daughters, there must have terrible fights over bathroom time!

Bryan Sykes named his seven daughters of Eve
based on the first letter of the haplotype designation
each already had. Example, haplotype U became
Ursala – he must have seen Bond girl Ursula Andress
in Dr. No recently.

Why would maternal inheritance of mtDNA be a good idea? Current theories hypothesize that this a mechanism by which only genetically strong sperm will reach the egg, and only genetically strong mitochondria will be inherited. With only a few mitochondria in the sperm, they must perform well in order for the sperm to reach the egg. If genetic mistakes have been made during meiotic production of sperm, then chromosomal errors might be accompanied by mitochondrial errors. A fast swimmer indicates a genome without harmful mutations. So the strongest genes get to the egg.

On the other hand, the effort to reach the egg means lots of ATP production, which also means lots of oxygen produced by oxidative phosphorylation. Oxygen can be damaging; the mitochondria probably aren’t in good shape at the end of the race. The sperm may be like salmon. The strongest make it up stream, but they end up so broken down that one trip is all they get; the damage would prevent the next round of their sperm from being prime material.

Why would evolution choose to pass on damaged paternal mitochondria when you have perfectly fine maternal mitochondria laying around in the hundreds of thousands. The chances are greater that the mother’s mitochondria are normal at this point, so the paternal versions are denied entry. Makes sense.

But some organisms just have to rock the boat. Blue mussels (family Mytilidae) and some freshwater mussels have two different types of mtDNA, called F and M – how original. The female passes on the F type to her sons and daughters, while the males pass on the M type to just their sons. Called doubly uniparental inheritance (DUI), females are homoplasmic (one type and males are heteroplasmic (two types).

Males are usually F type dominant in their somatic cells, but M type dominant in their spermatozoa. The females must be F type dominant in all cells, since they only have one type. The interesting part is that both male and female embryos get M type mtDNA, but in those destined to be females, the M type are degraded within 24 hours.

A 2009 study shows that the sex determination and inheritance of the male mtDNA are not coupled, and the female has complete control over whether the male type will be inherited and maintained. But there are occurrences of females with some M type, and males with only F type. Therefore, maternal inheritance is more stringent than DUI ------  Or is it?

This is a Schistosoma mansoni egg. It looks
like a cartoon bubble; I keep expecting it to
say something. S. mansoni is an exception
for trematodes, it has two sexes (is dioecious),
whereas most others are hermaphroditic.
The function of the spine on the egg is not known,
but it may help the egg stick to the wall of the blood
vessel in the host.
In some cases, like honeybees, mice, and a parasitic worm called Schistosoma mansoni, there can be “leakage” of paternal mtDNA into the fertilized egg. Even in some mammalian species other than humans, including sheep and mice, the tail of the sperm can penetrate the oocyte. This gives a zygote with many copies of female mtDNA and a few copies of paternal mtDNA. For some reason – I assume there is a reason, although I don’t know it -- this occurs more in crossbreeding (interspecific breeding – between species), than when two animals of the same species are bred.

In the breeding of animals of the same species, if there is paternal mtDNA present, it is degraded in the fertilized egg. Near the time of birth, they might have only a trace of paternal mtDNA left, but the mechanism by which this occurs is not known. During this time, there is the small chance that male mtDNA could recombine with female mtDNA and gum up the workings of strict maternal inheritance. In any case, there has been only one documented case of a paternal mitochondrion in a child, and this case was clouded by issues of infertility. Does this child feel disconnected from his great, great, great, great grandmother?

So much for animals - how about plant inheritance of chloroplasts and mitochondria? Do they follow the same rules – let’s find out next time.

Ellen L. Kenchington, Lorraine Hamilton, Andrew Cogswell1, Eleftherios Zouros (2009). Paternal mtDNA and Maleness Are Co-Inherited but Not Causally Linked in Mytilid Mussels PLoS One DOI: 10.1371/journal.pone.0006976

For more information or classroom activities on maternal inheritance, mitochondrial Eve, or fertilization, see –

Maternal inheritance –

Mitochondrial Eve –

Fertilization -

Thursday, December 28, 2017

When Is A Chloroplast Not A Chloroplast?

Biology concepts – gravitropism, plastid, chloroplast, chromoplast, amyloplast, leucoplast, malaria parasite

Believe it or not, the way plant roots know to grow into the dirt is related to photosynthesis! “How can this be?” you ask. Well, let’s talk about it.

The cells in the tips of the plant rootlet respond positively to gravity, called gravitropism (the older word for it is geotropism). If you lay a growing plant on its side, the roots will respond by growing (turning) toward the gravity within 10 minutes. The mechanism for this stimulation involves tension and a plant hormone called auxin.

Auxin is a growth hormone that gets redirected
in the growing plant root. The statoliths settle
and trigger the hormone to some cells more than
others. Auxin means ”to grow” in Greek, but in
some cases, like in gravitropism of roots, it
actually inhibits growth.
The root cap (the cells at the tip of the root) have some specialized cells called statocyte (stat = position, and cyte = cell). Inside the statocytes are dense granules called statoliths (lith = stone). The statoliths are made of densely packed starch and are a specialized type of organelle called an amyloplast, which is used in many plant cells for storing carbohydrate in the form of starch (amylo = starch). The statoliths are denser than the cytoplasm of the cell; they don’t just float around, they settle out according to gravity.

Since the statoliths are connected to the membrane of the cell by the cytoskeletal actin molecules, so when they settle toward gravity, some cells in the membrane are stretched and some are compressed. This tension signals the cells to change the number of receptors for the growth control hormone auxin. More tension (more stretch) causes the auxin to move away, toward cells that are under less tension. Auxin prevents cell enlargement and cell division, so those root tip cells on the bottom receive more inhibition. Those on top enlarge more and divide more, so the root turns down. If the root is already vertical, the tension is equal in all directions, and the growth is equal in all directions – the root gets thicker and longer.

Gravitropism is related to photosynthesis in that both mechanisms involve chloroplasts, sort of. Root cells don’t perform photosynthesis, they are underground, so they don’t have chloroplasts. But they do have the amyloplastid statoliths, and these are related to chloroplasts.

Both amyloplasts and chloroplasts are specialized versions of the plant organelle called the plastid. We asked last week about what defines a plant cell – maybe the plastid is it. All plant cells have some plastids, but in different plant cells they may take different forms, including chloroplasts, chromoplasts, leucoplasts, amyloplasts, elaioplasts, or proteinoplasts, but they all start out as proplastids (pro = early and plastos = form in Greek).

Proplastids are in every new plant cell. From there
they can differentiate into other forms, including
the chloroplast. Other plastids are used for storage
or biochemical production. We will talk about statoliths
again when we discuss proprioception.
When a cell divides, each daughter gets its share of proplastids, and then depending on the chemical signals that the daughter cell receives, the proplastid will differentiate (from latin, means to make separate) into the types of plastids that the cell needs. A proplastid can become any type of plastid, and from time to time can change between forms as the plant cell requires. Think of it as a sort of stem cell inside a plant cell – if the cell happens to be in the stem of the plant, it could be a stem cell inside a stem cell!

Proplastids become etioplasts, chloroplasts or leucoplasts. The etioplast is a sort of pre-chloroplast; a chloroplast without chlorophyll. It is waiting to be stimulated by light energy before it decides to spend all the energy it requires to make the chlorophyll. The old science fair project about growing bean plants in the dark demonstrates the etioplasts. The plants are white when grown in the dark, but bring them into the light and they soon green up. The sunlight stimulates the etioplasts to make chlorophyll, become full-fledged chloroplasts and start photosynthesizing.

This is a photomicrograph of the plastids of a
red flower petal. The chromoplasts hold the
xanthocyanin pigments, but we see it as a
continuous color because they are so small.

If the proplastid does not differentiate toward a chloroplast pathway (etioplast too) then it will become a leucoplast (leuko = white). The leucoplasts don’t have color; they become specialized for the storage of plant materials. If they store starch, they are called amyloplasts. Lipid storing leucoplasts are called elaioplasts, while protein storing plastids are called proteinoplasts. Each type serves a crucial purpose in the cells they inhabit, and they can all interchange, depending on the conditions the plant cell finds itself in.

Even more important, leucoplasts that are not serving as storage organelles have biosynthetic functions. They work in the production of fatty acids and amino acids. Amino acids link together to from proteins, so their synthesis is very important for plants. Plants must manufacture every amino acid it needs, whereas we get many of ours in our diet. There are even some amino acids that humans can’t make, called the essential amino acids. Of the twenty common amino acids, nine of them must be taken in through our diet, and some people with pathologies can’t make up to seven more. Plants don’t have this luxury; all their amino acids must be made on site. Good thing they have leucoplasts.

There is one other type of plastid that we haven’t talked about, the one that is important for the Autumn tourist trade. Etioplasts and chloroplasts can differentiate into chromoplasts, organelles that store pigments (colored molecules) other than chlorophyll. Chlorophyll provides energy through photosynthesis, but they also have a cost. The old saying, “It takes money to make money” applies to plants as well. It takes energy to make chlorophyll, so it only pays to make chlorophyll when there is ample sunlight to put through photosynthesis. When the days get shorter, the profit margin for producing chlorophyll goes down, so the plant just stops making it.

Twin females were imaged after a lifetime of smoking or non-smoking.   
Can you guess who was exposed to the oxygen radicals in cigarette
smoke her whole adult life?
The oxygen produced in plant cells during photosynthesis can damage many molecules; oxygen likes to react with other compounds and steal or donate electrons. This oxidative damage can wreak havoc with the cells, just look at the face of a long time smoker – the damage and aging process from the oxidants in cigarette smoke will be evident. The chromoplast pigments, like carotenoids (oranges and yellows) and xanthocyanins (reds and purples), can serve as antioxidants, and protect the other cell structures from the damaging effects of oxygen.

So the chloroplasts lose their chlorophyll in autumn and could be called leucoplasts, but the chromoplasts still have the pigments that had been masked by the greater number of chlorophyll molecules. The trees turn magnificent colors and bring people from the cities to stay in bed and breakfasts, and to purchase handmade scarves and way too much maple syrup and apple butter. Economy and biology are so often interrelated.

Plastids are the quintescential plant organelles – no plant cell is without them in some form (well O.K., there is one exception, we’ll talk about that next week). But that still doesn’t mean that they define a plant cell. Remember that algae are not plants, but they have chloroplasts, and chloroplasts are one type of plastid. There is even a bigger exception in this area; some of the apicomplexans.

Certain protozoal organisms, including the malaria parasite (Plasmodium falciparum) contain an organelle called an apicoplast. P. facliparum or its ancestor obtained an algae cell by secondary endosymbiosis (the primary endosymbiotic event was the algae taking in a cyanobacterium), so the apicoplast has a four, not two, membrane system.

The apicoplast of the malaria parasite is of plastid
origin, but it undergoes some unplant-like changes
during cell division. Image D with the branched
apicoplast is my favorite. Those in panel F will
grow to look the one in panel A.
The apicoplast does not perform photosynthesis; we aren’t exactly sure what it does – but it is crucial for the survival of the parasite. It is located in the front of the parasite (in the direction it moves and invades cells) and is always close to the nucleus and the mitochondrion. This suggests some role(s) in energy production and molecule synthesis.

There is evidence that the apicoplast works in fatty acid and heme synthesis, like the leucoplast or in the production of ubiquinones that are important for the electron transfer chain in the mitochondria. There is also evidence that it is involved in FeS cluster production, like the hydrogenosome and mitosome. Both of these pieces of evidence show the interelationships of the endosymbiosed organelles and the connection between energy production and energy use. Whatever their functions are, if you destroy or inhibit it the malaria bug dies. As such, it has been a popular target for anti-malarial drugs.

Malaria parasites cured of their apicoplasts (cured means freed of) do not die right away. They just can’t invade any new cells and therefore can’t complete their life cycle. This is why anti-apicoplast drugs may be a boon to malaria treatment. The biosynthetic pathways in the apicoplast are the targets of four recent drugs, but the primary way to stop malaria remains the mosquito net. There is strong hope that a new vaccine, called RTS,S is a light at the end of the tunnel for this killer of millions.
The melanosome and the plastid have more in common.
The very rudimentary eye of some dinoflagellates
(dinos = rotating, and flagellum = whip) has a melanin-like
molecule in the pigment cup and the structure is called a
melanosome. However, it is of plastid orgin. The picture
above is of Polykrikos herdmanae. It has 8 transverse flagella,
as well as the pigmented eyespot to detect light sources.

One final thought on the plastid – an addition to the exception of melanosomes. We discussed a few weeks ago that melanosomes were the only organelles that could move from cell to cell. Well, that isn’t exactly so. I held off on adding the plastid to that list until we had discussed what a plastid was.

A 2012 study at Rutgers University tested whether plastids and mitochondria could move between plant cells. There results showed that entire plastid genomes could be seen in recipient cells, and the fact that the whole chromosome passed indicated that the plastid was probably moving from cell to cell intact. But there was no movement of the mitochondria, so it is a plastid (and melanosome) specific event.  The researchers hypothesize that this may be a way for plant cells to repopulate damaged cells with working organelles. As such, it would be similar to how mammalian stem cells can move mitochondria into damaged cells during tissue repair. But that is another story.

We have repeatedly talked about how the mitochondrion and plastid can replicate on their own and then are portioned out to the daughter cells when a parent divides. Can it really be that simple? I’ll bet there is a definite mechanism, and I bet that mechanism has exceptions. Let’s look into this next time.

Gregory Thyssena,Zora Svaba, and Pal Maligaa (2012). Cell-to-cell movement of plastids in plants Proc Natl Acad Sci U S A. , 109 (7) DOI: 10.1073/pnas.1114297109

For more information or classroom activties on plastids, gravitropism, or Plasmodium falciparum see:

Plastids –

Gravitropism –

Plasmodium falciparum