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Different cultures have different practices when it comes to assigning middle names. I don't know the history behind any of it so I won't pretend like I do, but none of that actually matters now that I've invented a better system. Instead of naming the individual child, names are given to the sex chromosomes
(X and Y) and the child takes the name of the chromosomes. A child's paternal surname is that of the chromosome which he received from the father, while his or her maternal surname (or middle name, optionally hyphenated) is derived similarly from the mother.
The Y-chromosome is transmitted patrilinearly, so a son receives his father's paternal surname. Likewise, a daughter receives her father's X-chromosome, so her father's maternal surname becomes her paternal surname. Assigning the middle name is a bit trickier. A child receives one of his or her mother's X-chromosomes, so his or her middle name will be one of his or her mother's surnames. Deducing this requires some kind of genetic analysis, but such a procedure is easily affordable these days.
Of course, parents are free to tack on extra names for whatever ceremonial reason, but these two surnames plus the given name will serve as the individual's legal name when genetic screening becomes mandatory and we move further towards Orwellian Utopia.
Personal numbers as names
Personal_20Numbers_20As_20Names
Official names which reveal nothing about prejudicial characteristics [nineteenthly, May 05 2017]
Bioenergetic Constraints on the Evolution of Complex Life
http://cshperspecti...nt/6/5/a015982.full
includes - why mitochondria still have a genome. [Loris, May 11 2017]
[link]
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Now, you might be asking, "What about recombination between maternal X-chromosomes?" |
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Effectively this is what we did, in a sense (about to use
bits of our real names BTW, perhaps unwisely). The old
username [grayure] is formed from our surnames, which I
later changed because it meant there'd been two people
posting under one username, so [nineteently] is just me.
Our daughter's surname is Gray and our son's is Ure. The
same applies back up my family tree. However, I wouldn't
say it was X and Y so much as mitochondrial and Y. Also,
there would be a major misgendering issue for some
people. |
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I think people should only be given serial numbers and
have no other official name. I'll post a link in a second. |
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// people should only be given serial numbers and have no other official name. // |
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<Unfurls large "VOTE FOR NINTEENTHLY" banner> |
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Ta muchly [8th of 7], you are my poster child. |
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//Now, you might be asking, "What about recombination between maternal X-chromosomes?"// |
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But the solution is obvious.
Y chromosomes are pretty short and boring and basically don't recombine much, so a single short name will suffice.
X chromosomes are a decent length and carry a number of interesting genes. And they recombine in every female generation. So we we give X chromosomes a long name based on a series of combinable phonemes (or alternatively a number of concatenated short names, each from a unique list). Then when a baby is born we simply need to sequence or fingerprint its X chromosome to determine its maternal name. |
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This has the fringe benefit that we can circumvent the protracted gender naming issue (Mr vs Miss, Mrs, Ms, Miz etc).
Boys have a long and a short name, girls have two long names.
Turner syndrome girls have one long name, Trisomy X girls have three long names. Klinefelter syndrome boys have two long names and a short name, and XYY boys have a long name and a repeated short name. |
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Okay, this is my gender-neural take on that: name people
after the autosomes. Those vary in the same way as the X
chromosome and there's more to identity than gender. Why
not just forget the gender and use a checksum-based
version of the genome to name people? |
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But I still maintain I want numbers, not names. |
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Since I've done the 23andme analysis -- which held some cool
surprises, I did discover that I had a number of direct
descendant relatives on a haplogroup, that was kind of cool.
Hopefully they won't ask for any money. |
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Don't worry, chimpanzees consistently choose cigarettes, beer,
chocolate and bananas over negotiable currency. |
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But when they visit, it will be a wise precaution to remove the
radio antenna and windscreen wipers from your vehicles. |
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The genes associated with mitochondria are responsible for
the energy-production that mitochondria do. Those genes
are transmitted purely matrilinearly (via the ovum). |
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"Describe, in single words, only the good things that come into your mind about... your mitochondria." |
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//The genes associated with mitochondria are responsible for the energy-production that mitochondria do.// Yes and no. Literally yes, but most mitochondrial proteins are encoded by nuclear genes (can't remember if the mRNA gets imported for translation in the mitochondrion; or if the proteins are imported from the cytosol - I think it's the latter). Evolution is gradually moving genes from the old bacterial genome in the mitochondrion, into the chromosomes where they're safer. In a few hundred million years, they'll all be in the nucleus and the mitochondrion will lose its genome completely. |
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Careless. Should put them in a tea caddy and hide them under the mattress ... they'd be safe there. |
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//put them in a tea caddy// Interestingly, if you took all the mitochondrial DNA in a cat and laid it out in a straight line, the cat would die. |
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<sound of Borg Collective dispersing in all directions in search of a live cat> |
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<sound of feline yowling, blender noises and gleeful cackling> |
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You're right ! It stretches quite a long way, too .... |
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[Vernon]//The genes associated with mitochondria are responsible for the energy-production that mitochondria do.//
[Max]//Yes and no. ...[comments]...// |
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//The genes associated with mitochondria are responsible for the energy-production that mitochondria do. Those genes are transmitted purely matrilinearly (via the ovum).// |
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I'm not entirely clear on why Vernon said that. My best guess is that it's in response to:
//...Our daughter's surname is Gray and our son's is Ure. The same applies back up my family tree. However, I wouldn't say it was X and Y so much as mitochondrial and Y. // |
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Which looks perfectly fine to me.
...although of course there is the occasional nonmaternal exception. |
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//In a few hundred million years, they'll all be in the nucleus and the mitochondrion will lose its genome completely.// |
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I went to an interesting talk a while back which would suggest not. As I understood it, the regulation of expression of the genes remaining in the mitochondria is critical to avoid radical oxidative death. |
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Hmm - that's an interesting point. Certainly having the genes right there in the Mt would allow more immediate regulation in response to mitochondrial parameters. |
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[Loris], the Idea here is about naming children in a way
relating to genetic heredity. I was simply pointing out that
part of our genetic heredity is transmitted purely
matrilinearly, outside the DNA of cell-nuclei. |
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Actually you could combine the 10 genes highest interest, then make a version of childs name with that, then people would know a lot about each other from their names. With enough vowels it could sound nice. |
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Comv'Apab would start off the name of of a person with val val COMT (unreactive, abstract) who had longevity version of APOE-b So you know a part of their personality, along with that they have minimal risk of cardiovascular disease. |
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Why not just use a hash of their complete genome sequence? |
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//Why not just use a hash of their complete genome sequence?// That, [MB], was a stupid suggestion. For one thing, a single sequencing error would completely change the hash. For another, you couldn't back-compute from the hash to the genome sequence. And for yet another, no two cells in your body have exactly the same sequence, so you might end up naming someone after a scrotal skin cell. |
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Just run the ion-channel output of an Oxford Nanoporn sequencer direct to audio. It's probably about all that machine's good for. |
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A perceptual hash would work, though. |
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I guess that would result in something like using
phenotypes as names. |
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//In a few hundred million years, they'll all be in the
nucleus and the mitochondrion will lose its genome
completely.// |
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It hasn't happened yet, and it's had a while. If it was an
advantage, the generation time and numbers involved
with organisms such as yeast would have got there
already. In fact it looks like we're at steady state. |
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//I went to an interesting talk a while back which
would suggest not. As I understood it, the regulation of
expression of the genes remaining in the mitochondria is
critical to avoid radical oxidative death.// |
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No. Probably not, it makes total sense which is why its
almost certainly wrong. |
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My first thought on why the mito genome was still around
was based on the huge variability in demand for oxidative
phosphorylation from cell to cell. Take a cardiomyocyte,
a heart cell, that's almost ALL mitochondria, working all
the time. So they need lots of copies of the proteins that
do the oxidative phosphorylation. Great, each mito has
100s of copies so a heart cell has 20,000 or so
mitochondrial chromosomes, whereas an epithelial cell
that's just sort of sitting about, has a few hundred. |
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At this point I thought "fine, that's the answer, change
the copy number of mitos and their genomes and you can
scale expression by thousands of fold to meet the wide
range of bioenergetic demands that different cells and
tissues have (there's a type of cell that lives in the
intervertebral discs that have no mitochondria, they're
weird) all while getting away with only one nucleus. It
would be a real pain to have an extra 20,000 copies of
the oxidative phosphorylation genes in the nucleus of
every cell just in case one decides to be a heart cell" |
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Except that's wrong-headed Friday night thinking.
Monday morning thinking suggests that the protein
COMPLEXES involved in mitochondrial oxidative
phosphorylation are a mix, derived from both the mito
and nuclear genome. So the nucleus can clearly supply
the necessary amount of proteins to keep up with the
demands of even a cardiomyocyte. |
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My next clever thought was "ah, but the proteins coming
from the mito genome are enriched in those weird,
dangerous iron sulphur complexed things, I bet they're
damaged, degraded and replaced at 10-100 times the
rate of the proteins from the nucleus, so you need local
enrichment of genes to keep up! we're back to that lovely
scaling idea I had!" |
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Nope. Proteins within the same complexes degrade at the
same rate independent of their chromosomal origin. |
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So, my not disproved yet theory is that the mitochondria
represent a population within a cell. As such, they're
subject to natural selection (enhanced significantly by
the cell's degradation machinery) and evolution at a rate
independent of the rest of the cell/organism. You don't
need all of the genes in the mitochondria to do this. Just
a representative smattering from each important
complex. |
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With that, the environment runs selection/evolution in
nested layers population> organism> cell> organelle. In
response to selected environments, the organism can
adapt faster than should be possible. Even in humans the
mitochondria show evidence of this, central Africans have
tightly coupled non-leaky mitochondria, efficient ATP
generators. Northern populations have slacker leakier
mitos, since a little heat generation is an advantage.
Would be fun to look at the people who go work in
Antarctica, since their calorie expenditure jumps up just
because of the cold. |
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You know, [bs], you should take up this biology malarkey professionally. |
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The idea of mitochondria evolving as a subpopulation within, yet quasi-independently of, the cell is intriguing. It's interesting especially because the environment of each population of mitochondria is limited to one cell (or a few generations of cells), so there's the potential for independent evolutionary trajectories in each cell or in each cell type. Of course there's then a population bottleneck every time the host human reproduces, so you'd expect to have a sort of recurring (on human generational timescales) mitochondrial evolution. |
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What would be really, really cool would be to sequence mitochondria from the oocyte (or, perhaps easier, from the first or second polar body, if they contain any), and then sequence single mitochondria from multiple tissues in the same individual as they grew up. It would probably need a whole-body biopsy to get really complete data, but you can't make an omelette etc. |
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I considered using the mitochondrial chromosome instead of the X chromosome to record maternal lineage. This has the advantage of removing the requirement for genetic testing to determine the surname, but it also means that girls wouldn't get a paternal surname. Provided we kept at it long enough, another feature of doing it this way is that there would eventually only be two surnames left in existence: those of Mitochondrial Eve and Y-chromosome Adam. |
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Also, that is an interesting hypothesis regarding mitochondrial evolution. While some might speculate that this could be a way for the individual to adapt to its environment (over years or decades), what I think you have here is an evolutionary crystal ball that allows the population to see many generations into future based on the performance of the individual. Any evolution that happens inside the environment of the cell over the lifespan of the individual organism is not "saved" to the population, because the only mitochondrial chromosomes that can be passed on to the next generation of organisms are those in the ova of the female. Ova are created during gestation and, as far as I know, they exist from birth until menopause. |
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This doesn't mean that the evolution that happens over the course of the individual's lifetime is for nought, however. Even though some beneficial mutation that occurs during the lifetime of the individual won't be saved to the population's gene pool, the PROPENSITY for generating that beneficial mutation at some time in the future will be. For example, if some mutation initially manifests itself in the mitochondria of a 6-year-old child's heart cell which then spreads to a significant chunk of his heart so as to substantially alter his reproductive fitness (either beneficially or deleteriously), then the population will know that it is very close to "locking-in" this mutation to the population's gene pool because whatever genotype that exists in the ova of its females is very close to the mutation that manifested itself in the individual. For this to work, (1) the effects of the mutation MUST BE FELT IMMEDIATELY, BEFORE the organism reproduces, and (2) whatever process causes mutations to occur over the lifetime of the individual must also operate when ova divide. Effectively, this mitochondrial evolution mechanism allows the population to put out evolutionary feelers; to try before it buys, as it were. |
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As a simplified example, say that each female carries 1000 eggs, each adult human has a trillion cells, and every cell in the body has the same number of mitochondria. Then this means that there are about a billion times more mitochondrial replications over the lifetime of the individual than there are during gestation when whatever progenitor cell produces all of the female ova. If it were the case that a super-mitochondrion could automatically identify itself and immediately replace every other mitochondrion within the body of the organism, this would mean that the individual effectively samples mitochondrial evolution one-billion human generations into the future. |
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Of course, it doesn't work this way; not all mutations in the mitochondrial genome will be equally impactful on the reproductive fitness of the individual organism and this largely depends on where and when the mutation occured. A mutation that occurs during generation of the ova is going to be far more impactful than one that occurs in a scrotal skin stem cell, for example. What you could do though, is to score each mutation by impactfulness as a function of the stage of development where the mutation occurred, the tissue in which it occured, and the mutation itself. By taking the ratio of the aggregate impact-score of all mutations that occur over the lifetime of individual (from zygote until post-reproductive age) to that of all those that occur from ova progenitor cell to ova, you will get the number of human generations of mitochondrial evolution that the individual organism is able to preview. |
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Theoretically, this scheme need not be restricted to genes that function in the mitochondrion. Any gene whose evolution that the organism wants to accelerate could be sent to the mitochondrial R&D labs for a few million years and then imported when it's improved. |
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"And what's your surname?" |
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"AATAAAGAATCACCGTCTAAATCGT..." |
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"I'm sorry, how do you spell that again?" |
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//only mitochondrial chromosomes that can be passed on
to the next generation of organisms are those in the ova
of the female. Ova are created during gestation and, as
far as I know, they exist from birth until menopause.// |
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Whenever I see "exclusively", "only", "ever", "always" my
did you realise you're dealing with biology? o-meter goes
off the scale. The exclusivity of matrilineal mtDNA
inheritance is definitely not a thing <link>. I leaned my
lessons in the early days of my molecular biology
undergrad when they were still teaching the "central
dogma" of DNA > RNA > Protein. |
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// adapt to its environment (over years or decades)//
Hours, potentially. That's how long it takes a few percent
lower glucose to start fusing the mito network. Then
there's other layers of regulation, mtDNA is subject to
epigenetic modification, and there's plenty of evidence
that cells donate mitochondria to others. I think if you
sequenced a whole lot of mtDNA from a pair of mice and
put them in different heat/cold lazy/exercise
environments or fed them differently, you'd see a shift,
probably reversible. |
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//You know, [bs], you should take up this biology malarkey
professionally.// |
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or take the pay increase associated with the same number
of hours non-professionally, but where's the fun in that? |
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Hmmm. Mitochondrial evolution seems to be the topic of the moment. |
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////I went to an interesting talk a while back which would suggest not. As I understood it, the regulation of expression of the genes remaining in the mitochondria is critical to avoid radical oxidative death.//
//No. Probably not, it makes total sense which is why its almost certainly wrong.// |
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I exaggerated for comic effect, but the evidence given in the talk seemed plausible. |
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//So, my not disproved yet theory is that the mitochondria represent a population within a cell. As such, they're subject to natural selection (enhanced significantly by the cell's degradation machinery) and evolution at a rate independent of the rest of the cell/organism. You don't need all of the genes in the mitochondria to do this.// |
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I'm not at all convinced by that.
IIRC mitochondria are more prone to mutation, but that's probably for practical reasons, rather than an intended effect. The selection of mitochondria intra-cell is likely all going the 'wrong way'. As a mitochondrion, you probably don't get a pat on the head and told to replicate for doing a good job. And mutations are unlikely to be beneficial at the best of times. |
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Anyway, I looked up the talk I went to. It was by Dr Nick Lane, and was quite wide-ranging. Title was :"How Deep Evolutionary History can Affect Human Health".
I don't want to go too much into the details of this because I wouldn't do his chain of logic justice, and might get some of it wrong. But he's written several books (which have won awards apparently), as well as scientific papers, so they're an option if you want to get the full description.
Nevertheless, he did mention that he thinks the mitochondrial bottle-neck is deliberate; the idea is to give each offspring a clonal population so that you have a chance of getting a good copy. The ones with dubious versions do badly, but that's better than giving everything a mixture because then selection doesn't get to act on them and your decendants get worse with every generation. For larger multicellular animals, terminating dodgy embryos early is an option. |
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I have received my X chromosome.. |
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//I exaggerated for comic effect, but the evidence given
in the talk seemed plausible// |
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I work in the field of reactive oxygen species/redox and
mitochondria and there is a mountain of dreadful science
out there. There's also a stack of tired old received
wisdom, and an equal amount of knee-jerk reaction from
people like me. Anyhow, I don't know the guy. I'll take a
look and get back to you, that wont be fast, but it will be
good for me, I think every experiment should have at
least some interpretation in the context of evolution and
selection. |
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//regulation of expression of the genes remaining in the
mitochondria is critical to avoid radical oxidative
death.// |
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uuughhhh I'll see if I can explain briefly while making
sense. The large protein complexes (not complex 2) in
mitochondria that can produce reactive oxygen species
are made of nuclear and mitochondrially derived
proteins. So you can regulate the mitos all you like, but
the function requires nuclear cooperation. (Conversely a
mutation on the nuclear genome of one or several
mitochondrial proteins will convey dysfunction on the
mitochondria, which is overlooked). So, the big question,
which wasn't a question until it began to be answered, is
how the two genomes cooperate to get the right protein
ratios. There's a recent Nature paper that suggests this is
done nucleus>mito and regulated at the translation level. |
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Anyhow, it's best not to think of mitochondria as reactive
oxygen species producers. It's best to think of the cytosol
and the mito matrix as environments that are actively
maintained in an artificially reduced state. In both
environments, there is a sea of reduced glutathione that
several sophisticated families of enzymes that mostly
keep everything reduced. Next in the chain (there are no
antioxidants, just a sliding scale from reducing (food) to
oxidizing (oxygen) the difference between those is just
like two terminals on a battery that is used to power all
the fancy ion pumping we call life) is NADPH. There's a
couple of ways this is made in the cytosol, mostly
requiring glucose, but the mitochondria pull a trick with a
wonderful enzyme called Nicotinamide Nucleotide
Transhydrogenase. And the H+ pumping machinery needs
to work to power that. |
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Anyhow, my point is that everything will oxidize horribly,
and potentially locally, if you don't maintain it. So
"radical oxidative death" is probably better stated as
"failure of the active redox management system". I think
the retention of the mito genome isn't explained by that,
after all, the ER is a complex, necessary organelle with
all kinds of fancy redox equipment and ion channels the
size of buses and the nucleus manages that just fine. |
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//radical oxidative death// That's how I'd like to go. It sounds so spectacular. |
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[+] Ladies before Gentlemen. |
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I have found a paper which has his argument for why mitochondria retain their (residual) genomes: Bioenergetic Constraints on the Evolution of Complex Life (Nick Lane; Cold Spring Harb Perspect Biol 2014;6:a015982)
I will link to it, and quote the relevant part below. It's under the subheading "The Requirement for Core Bioenergetic Genomes" |
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>" ... Mitochondria never lost their genomes altogether, except when they also lost the capacity for respiration (van der Giezen 2009). Their core genomes invariably encode the same group of membrane-integral respiratory proteins, plus the ribosomal and transfer RNAs needed to express them locally (Gray et al. 2004). The most compelling explanation for the retention of these genes is that because local transcription and translation enable a swift, proportionate response to shifts in substrate availability, oxygen tension, and free-radical leak, maintaining effective coupling of electron flow to ATP synthesis, as argued by the CoRR (co-location for redox regulation) hypothesis (Allen 1993, 2003). Local transcription is indispensable in the mitochondria, but not in other membrane systems such as the endoplasmic reticulum (ER), because the costs and benefits are much greater, while the time window is far shorter. Mitochondrial membrane potential is 150–200 mV, and the membrane is ~5 nm thick, giving a field strength of 30 MV/m, equal to a bolt of lightning. The penalty for losing control over this colossal electrical potential is collapsing ATP availability, high rates of free-radical leak, and cell death. Mitochondrial genes are expressed in response to local (matrix) changes in free-radical leak, which modulate redox-sensitive transcription factors such as mt topoisomerase-1 (Lane 2011b), via oxidation of protein thiols (F Boege, pers. comm.). This can correct for imbalances in electron flow in a matter of minutes, where and when needed, staving off cell death for a little longer. Suffocation at the organism level takes minutes; failure to control respiration in the mitochondria carries an equally swift and lethal penalty." |
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