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