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

digits.

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 –

http://www.woodrow.org/teachers/bi/1997/apotosis/

http://www.lessoncorner.com/Science/Biology/Cell_Biology/Apoptosis

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC256977/

http://www.ehow.com/how-does_5172524_steps-apoptosis.html

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/Apoptosis.html

http://www.youtube.com/watch?v=wREkXDiTkPs&feature=fvwrel

http://www.cellsalive.com/apop.htm

http://www.celldeath-apoptosis.org/

http://www.promega.com/resources/product-guides-and-selectors/protocols-and-applications-guide/apoptosis/

www.roche-applied-science.com/PROD.../apoptosis_003_004.pdf

http://abstracts.aspb.org/pb1997/public/P64/0400.shtml

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CHYQFjAA&url=http%3A%2F%2Fjcmb.halic.edu.tr%2Fpdf%2F4-1%2FProgrammed.pdf&ei=9R7eT5ebCoim8gSK-pj3Cg&usg=AFQjCNEscW4eeiFGAzLuSE-mQAhR_xF3lw

www.plantsciences.ucdavis.edu/faculty/durzan/146.pdf

Synaesthesia –

http://faculty.washington.edu/chudler/syne.html

http://web.mit.edu/synesthesia/www/

http://synesthete.org/

http://www.mixsig.net/

http://nookkin.com/content/synesthesia.php

http://www.quibblo.com/quiz/1fOzV6O/Do-You-Have-Synesthesia

http://matthewjamestaylor.com/blog/synesthesia-associating-colours-to-letters

http://www.enotes.com/documents/synesthesia-worksheet-1139

http://www.psychologyinaction.org/2011/01/28/synesthesia-when-ordinary-activities-trigger-extraordinary-sensations/

http://www.awaytoteach.net/?q=node/5128&quicktabs_2529=0&quicktabs_2530=3

https://sites.google.com/site/synesthesiaresearchteam/

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 –

http://www.saylorplants.com/SaylorPlants/Ref_Info/Dioecious2w.htm

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CEkQFjAA&url=http%3A%2F%2Foklahoma4h.okstate.edu%2Flitol%2Ffile%2Fothers%2Fenrichment%2F4h500.pdf&ei=aXvKT4TuMIeC2wW1q4HaCw&usg=AFQjCNGyz1D_o5uVX0nMrNa2VpjchuJHgw

http://botany.csdl.tamu.edu/FLORA/Wilson/pp/s99/flowers.htm

http://www.oakleafgardening.com/glossary-terms/hermaphrodite-monoecious-dioecious/

http://www.bushmansfriend.co.nz/dioecious-plants-xidc18308.html

Angiosperms –

http://www.ehow.com/info_8462298_classroom-activities-angiosperms.html

http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=9&ved=0CHIQFjAI&url=http%3A%2F%2Fwww.burpeehomegardens.com%2Fpdf%2FBHC10538-BurpeeICanGrow-PlantClassification.pdf&ei=vn3KT5-dNMnW2gXOjc3ZCw&usg=AFQjCNH5IaI0aDUM1qd4wj_tVEaF-o8-jw

http://alex.state.al.us/lesson_view.php?id=24127

http://www.teachervision.fen.com/seeds/printable/28684.html

http://beckyboop.wordpress.com/2011/04/05/flowering-plants-lesson-plan/

https://www.google.com/#hl=en&sclient=psy-ab&q=gymnosperms+and+angiosperms&oq=gymnosperm&aq=1&aqi=g4&aql=&gs_l=serp.1.1.0l4.50243.54373.3.55834.20.16.1.1.1.13.328.3452.0j9j6j1.16.0...0.0.2xyYaWj6zCc&pbx=1&bav=on.2,or.r_gc.r_pw.r_qf.,cf.osb&fp=9d6464494833eb73&biw=1689&bih=895

Gymnosperms –

www.clt.astate.edu/mhuss/Lab%20Exercise%2011.doc

http://faculty.unlv.edu/landau/gymnosperms.htm

http://www.gardenbuildingsdirect.co.uk/Article/gymnosperms

http://alex.state.al.us/lesson_view.php?id=24115

http://sfr.psu.edu/youth/sftrc/lesson-plans/forestry/6-8/gymnosperms

http://academic.kellogg.edu/herbrandsonc/bio111/gymnosperms.htm

http://faculty.clintoncc.suny.edu/faculty/michael.gregory/files/bio%20102/bio%20102%20lectures/seed%20plants/seed%20plants.htm

http://www.msnucleus.org/membership/html/k-6/lc/plants/5/lcp5_5a.html

Plastid inheritance -

http://www.ncbi.nlm.nih.gov/pubmed/20052516

http://www.amjbot.org/content/94/1/42.full

http://www.generationcp.org/plantbreeding/index.php?id=015

http://www.clivias.com/Articles/Article016.htm

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 4^th 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 50^th generation mtDNA necessarily looks different from the 1^st 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 50^th 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 –

http://www.ndsu.edu/pubweb/~mcclean/plsc431/maternal/maternal2.htm

http://www.as.wvu.edu/~kgarbutt/QuantGen/Gen535_2_2004/Maternal_Inheritance_3.htm

http://www.dnalc.org/view/15977-Maternal-inheritance.html

http://hitechbloodstock.com/mitochondrialdna.htm

Mitochondrial Eve –

http://www.pbs.org/wgbh/nova/neanderthals/mtdna.html

http://www.sciencedaily.com/releases/2010/08/100817122405.htm

http://syllabus.med.unc.edu/yr4/gen/medhist/publish/mitochnotes.htm

http://www.mhrc.net/mitochondrialEve.htm

http://www.archaeology.org/9609/abstracts/dna.html

http://io9.com/5879991/the-scientists-behind-mitochondrial-eve-tell-us-about-the-lucky-mother-who-changed-human-evolution-forever

http://blog.oregonlive.com/my-beaverton/2012/04/whos_your_mama_is_it_mitochond.html

http://www.discoveryeducation.com/teachers/free-lesson-plans/the-real-eve.cfm

http://www1.umn.edu/news/features/2012/UR_CONTENT_372562.html

http://www.actionbioscience.org/evolution/ingman.html

http://www.designedinstruction.com/learningleads/mitochondrial-eve.html

http://www.aetv.com/class/admin/study_guide/archives/aetv_guide.0014.html

http://www.pbs.org/wnet/facesofamerica/lessons/i-dream-of-genome/lesson-activities/202/

http://science.howstuffworks.com/environmental/life/evolution/female-ancestor.htm

Fertilization -

http://www.vivo.colostate.edu/hbooks/pathphys/reprod/fert/fert.html

http://biology.about.com/od/genetics/a/aa040805a.htm

http://www.visembryo.com/baby/1.html

http://www.youtube.com/watch?v=6kGN2dcjNUY&feature=fvwrel

http://www.embryology.ch/anglais/dbefruchtung/akrosom02.html

http://www.biology-online.org/articles/vitro_evaluation_frozen-thawed_stallion/sperm_oocyte_interactions.html