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This week we bring you the news
that the entire human genome has finally been sequenced.
You’d be forgiven for thinking
“wait a second, didn’t we do that Like, twenty-ish years ago?”
We did, to much fanfare.
The Human Genome Project,
which set out to map every last piece of the human genome, was declared essentially complete
in 2003.
Here, however, “essentially complete” means “complete
except for the parts we’re content to ignore.”
See, in actuality, there were some huge gaps in the data.
Around eight percent of the genome was missing!
And that’s not because we didn’t know it existed;
it’s because the Human Genome Project focused on euchromatin.
These are regions of the genome that sit together in a nice loose little package
which is relatively easy for sequencing technology to unpack and have a look at.
It tends to include most actual genes, or regions of DNA that code for protein.
What the project left behind, though, was data on heterochromatin.
Heterochromatin is a tightly wound part of the genome
that hangs out more to the sides of the nucleus than euchromatin,
and contains fewer protein-coding genes.
Instead, it includes a lot of ends and middle parts of chromosomes
with a lot of repeated sequences.
It’s often thought of as ‘junk DNA’.
Euchromatin was easier to analyze with the tools available at the time,
and though plenty of scientists were interested in heterochromatin,
the complexity of decoding it made it less of a priority.
But now, with this new paper published in the journal Science,
we finally have a fully sequenced genome, complete with heterochromatin.
This most recent sequencing used newer methods
which can read much longer sequences at once.
Most sequencing methods can’t read a whole chromosome from start to finish,
but have to look at smaller sequences and paste them together where they overlap.
Longer sequences means fewer gaps to work out.
It also means you’re more accurate when dealing with repetitions than older methods,
because if a sequence is just one long set of repetitions,
it can be tricky to figure out the exact point where those separate parts overlap.
The result of the research team’s efforts is the 3.055 billion base-pair sequence
published in the team’s new paper.
This study also presents some new genes and other functional regions in the 8% they filled
in.
And this isn’t just a nice-to-have sequence of useless DNA.
Because heterochromatin definitely isn’t just junk.
In fact, many researchers believe that it’s heavily involved in organizing the genome,
controlling which genes are expressed,
which are silenced, and even helping with DNA replication and repair.
The team is hoping that having these regions sequenced
will fill gaps in our understanding of how many diseases develop, including even cancer.
[SEHN-troh-meer] Cancer is often associated with abnormalities
at the centromere,
which is the middle region where pairs of chromosomes join.
If we can get a better understanding of what’s going on there at a genetic level,
it may give us a new entry point to developing cancer treatments.
So hopefully this is just the start of some big advances in our understanding of our genome.
–
That’s not the only good news for cancer research this week.
On April 7th, researchers from Westlake University, China,
published a paper on how bacteria contribute to the spread of cancer.
While genetics and the environment are among the first ports of call for cancer researchers,
the team was still surprised by the role that microbes might play in tumor development.
That’s because scientists originally thought
that most tumors were sterile, containing no bacteria at all.
In more recent years, though,
bacteria have been cataloged in many different types of tumors,
with each type having their own distinct microbiome.
But this new work demonstrates
that microbes colonizing cancerous cells don’t just hang out.
They may actually have a big role to play in the ease
with which those cells can spread around the body.
In their study, the team used a mouse model of human breast cancer
with a significant amount of bacteria inside, similar to what you would see in human breast
tumors.
They observed that the microbes were present in tumor cells
that spread through the mice’s circulatory systems.
Not only that,
but they were actually making those cancer cells more resistant
to the rough and tumble of traveling.
The bacteria helped the cells reorganize their cytoskeleton,
which provides support for the whole cell, making them more likely to survive the journey.
Disrupting these bacteria resulted in reduced amounts of metastasis.
In other words, the circulating tumor cells
were less able to travel and establish themselves elsewhere in the body.
And while that didn’t affect the growth of the original tumor,
this discovery may provide new routes for cancer treatments.
Though the team doesn’t believe it’ll be as simple
as prescribing something like an antibiotic,
it could be that managing these bacteria may in future
help us keep cancers from spreading.
But that will be a little while yet.
This research was conducted in a mouse model,
so we don’t know if it’ll be the same in humans right now,
and it’ll take some time to get that research rolling.
For now though, we can be grateful to have another vital piece of the puzzle.
Thanks for watching this episode of SciShow News,
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