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From YouTube: DevoWorm #41: Making a Statistical Mask, Origins of Early Life, Minimal Cells, Autocatalytic Sets
Description
Creating a statistical mask from distributions. Modeling the origins of life with Braitenberg Vehicles. Mathematical modeling of autocatalytic sets for innovation and origins. Minimal cells and simulating whole bacterial cells, putting cellular components together into a whole. Attendees: Richard Gordon, Morgan Hough, Susan Crawford-Young, Jesse Parent, Bradly Alicea, and Morgan Hough
B
A
I
know
it's
going
to
be
hard
to
get
people
from
corralled
at
any
one
time.
I
don't
know.
B
It's
it's
crunch
time
for
students,
yeah.
A
B
A
I,
don't
know
yeah
I,
don't
know,
I
mean
I,
guess
you
can
just
keep
sending
emails
to
people
and
but
I
don't
know
if
they
respond
people
just
yeah,
it's
gonna
be
kind
of
tough
to
coordinate,
people
are
busy
doing
things
and
the.
B
A
A
One
group
and
then
transfer
to
another.
You
know
transfer
that
what
you
did
to
another
group,
like
oh
yeah,
like
just
basically
have
a
summary
of
what
was
done
and
that.
A
B
My
daughter-in-law
does
that
for
a
living
herding,
cats
yeah,
she
has
a
bunch
of
group
homes
that
she
looks
after
trying
to
keep
everybody
in
mind.
Okay,
I've.
C
I
could
help
you,
okay,.
A
A
I,
it's
I've
been
doing
some
stuff
with
some
of
the
things
that
we've
been
working
on.
I'll
share
my
screen
on
this,
so
the
first
thing
I
have
is
this
demo
of
embedding
elements
and
noise
I'm
not
sure
this
is
what
we're
thinking
about,
but
I
was
working
with
scilab,
which
is
a
program,
that's
kind
of
like
Matlab
you,
you
know,
but
it's
open
source.
So
you
can
work
on
matrices
and
transforming
matrices
and
I've
been
doing
this
noise.
A
Embedding,
but
I've
also
been
doing
some
of
the
stuff
from
the
tensegrity
book
in
scilab
and
trying
to
play
around
with
that
which
actually
has
worked
out.
I've
been
able
to
get
that
code
to
run
the
tensegrity
book
that
you
actually
pointed
out.
Yeah.
A
Code
in
there
for
a
different
right
like
taking
a
matrix
describing
a
tensegrity
network
in
terms
of
the
forces
and
then
getting
like
a
rank,
and
it's
like
you
know,
doing
Matrix
calculations
and
getting
an
output
like
a
rank
of
different
matrices
and
then
plotting
that
out.
Yeah.
B
A
You
can
put
in
any
set
of
values
for
The
tensegrity
Matrix,
but
it's
usually
you
know,
I
mean
you
can
make
comparisons
between
matrices.
So
if
you
say
this,
Matrix
represents
the
structure,
and
this
is
these.
Are
the
forces
and
you
get
like
something
at
the
end?
That's
a
that's
like
a
rank
of
The
Matrix,
and
so
it
it
gives
you
a
measure.
A
A
Certain
aspects
of
the
physics
so
like,
if
there's
something,
there's
a
there's,
a
dynamic
tension,
it's
like
one,
if
it's
neutral,
it's
zero
and
if
it's
not
it's
negative
100.
So
it's
like
at
each
node,
there's
a
certain
property
to
that
node.
If
it's
in
Dynamic
tension
or
not
I
can't
remember
other
Criterion,
but
that
I
mean
it's
very
pretty
easy
to
follow
through
you
just
put
some
put
in
a
matrix
and
you
can
get
a
a
measure
at
the
end
and.
B
A
Not
well
I
mean
it
does
most
of
the
things
now
it
does
everything
Matlab
does,
except.
A
Of
the
simulation
stuff-
but
you
know
the
it
but
but
the
book
from
the
the
code
from
the
book
works.
So
that's
it.
B
A
So
this,
okay,
let
me
go
through
this
yeah,
so
this
is
a
poisson
distribution.
This
is
actually
just
you
know:
defining
a
poisson
distribution
in
terms
of
its
gamma
value,
which
is
kind
of
like
it's
descriptive,
parameter
and
higher
the
descriptor
parameter.
The
more
points
you
get
going
like
kind
of
up
so,
like
you
know
the
lower
the
gamma
it
it
kind
of
resembles
gaussian
distribution,
the
higher
the
gamma
you
get
more.
A
You
get
more
higher
values,
more
points,
and
so
you
get
this
this
type
of
puts
on
distributed
signal
here.
So
that's
what
I
have
plotted
out
here
over
10
000
points,
so
these
are
just
points
that
are
generated
by
this
function.
This
is
a
random
generator
function
for
poisson
distributions.
It's.
A
So
this
is
the
poisson
signal
that's
out
in
the
world,
and
then
this
is
where
there's
some
noise
uniform
noise,
that's
generated
these
Green
Dots,
and
so
these
are
generated
and
I
can
plot
them
over
the
poisson
to
hide
those
points.
So
the
blue
points
are
my
poisson
points
that
I
generated
in
this
step,
and
then
here
I've
generated
Some,
Noise
overlaying
this
these
poisson
points,
and
so
it's
hiding
some
of
the
outlier
points
here.
A
A
A
But
yeah
yeah
there
are
a
lot
of
them
there
so
and
then
so,
they're
just
circles,
and
then
these
are
also
circles
he's
green,
but
because
there's
so
many
of
them.
You
know
you
get
this
field
of
it's
like
a
green
field
over
these
blue
circle
lines
and
then
sort
of
embeds
it
and
you
you
know,
I
was
like
playing
around
with
the
aspect
ratio
of
the
image,
and
so
you
can
get
like
more
crowding.
A
C
A
So
it's
it's
just
that
it
goes
from
left
to
right.
So
it's
generating
things
in
time
and
the
idea
is
that
it's
like
they
call
them
arrivals,
sometimes
in
in
poisson
distributions.
But
if
you're
measuring,
like
a
calculation
of
how
many
things
You
observe
at
a
certain
time.
So
it's
like,
if
you
think
about
like
a
highway
where
you're
standing
in
an
overpass
and
you're
okay,
how
many
cars
pass
in
like
a
minute
and.
B
C
A
B
A
A
Distribution
of
points
and
then
that
that's
overlaying,
the
poisson
distribution
so
you're
hiding
some
points,
they're
less
frequent
in
the
poisson
distribution,
but
the
more
frequent
points
that
occur
are
you
can
see
through,
and
so
the
point
of
this
then
is
to
have
like
this
mask
over
the
the
distribution
with
the
uniform
mask
that
you
know
kind
of
hides
some
of
those
points.
And
then
that's
that's
what
I
guess
we
wanted
for
detecting
points
out
of
the
back
road.
C
A
I
could
I
could
make
one
like
that,
I
mean
it.
Would
it
would
you
know
you
could
generate
it
the
same
way
and
it
would
look
a
little
bit
different,
but.
C
A
Well,
we
wanted
to
create
a
mask.
We
wanted
to
create,
like
signals
been
embedded
in
some
sort
of
noise
or
mask
so
this
is
the
this
is
the
uniform
distribution
that
would
be
like
the
noise
mask
and
then
the
the
poisson
distribution
is
underlying
that.
A
C
Could
be
what
it's
sort
of
a
spatial
Court,
in
other
words
you're
a
given
amount
of
time
you
switch
to
different
distribution
yeah
and
the
questions
that
you
did.
That
would
show
up
on
here.
C
C
A
A
A
They
did
I
was
looking
into
purlin
noise,
they
don't
have
it
in
the
grand
function
and
it's
a
little
bit
more
complex,
but
I
I
have
I
think
it
might
work,
I'm,
I'm
working
on
it
inside
lab.
It
would
be
nice
if
it
did,
because
you
could
actually
run
it.
It's
a
procedural
thing,
so
it
would
require
like
building.
C
C
A
A
And
this
is
where
it
now,
this
distribution
that
you
see
here,
which
is
a
poisson
distribution,
that's
been
sort
of
permutated
and
transformed,
so
that
most
of
the
signal
is
down
at
the
bottom.
So
it's
from
that
distribution
between
permutated
and
so
now,
I
have
a
band
at
the
bottom.
Where
you
can
see
it's
a
little
bit
more
visible
and
you
can
do
things
like
that
or
you
can
do
another
one
where
there's
a
band
at
the
top.
It's.
C
A
A
We
I
we've
gone
over
it
a
little
bit
and
I'm
going
to
go
over
the
paper
on
you
know:
I've
been
working
on
the
bradenberg
vehicle
section
kind
of
making.
I
don't
have
that
version
on
on
this
open
here,
but
I'm
working
on
some
of
the
details
in
terms
of
how
this
might
work,
how
we
might
be
able
to
like
the
parts
list
and
and
how
to
make
that
sort
of
more
Salient,
because
we
had
I
know
I
sent.
B
A
C
Okay,
good
yeah,
okay,
yeah
that'll
be
interesting
to
see
how
many,
how
many
random
structures
actually
function:
yeah,
yeah,
okay,
okay,
I'm,
not
sure
what
the
Criterion
is,
because
you
know
with
living
organisms.
Let's
say
microorganisms:
you
can
get
weird
mutants
that
go
around
in
circles
or
make
patterns
and
do
all
sorts
of
things
other
than
swim.
Normally
right
and
I
guess
you'd
still
call
them
alive,
yeah,
it's
just
that
they
they
have
a
different
function
in
life.
Yeah.
C
A
C
Know
that
you
know
like,
like
we
heard
a
crazy
guy
who's,
does
the
he
throws
himself
to
the
magnetic
reversal
group,
but
with
Magnetic
Universal
what
you
call
it
like
that
start,
a
podcast,
because
you
can
see
them
yeah,
but
he
was
reporting
on
a
bunch
of
sheep
that
go
around
in
circles
all
the
time.
Oh
yeah,
no
he's
not
he's
attributing
this
to
changes
in
the
magnetic
field,
whereas
it's
a
well-known
disease
in
sheep.
C
C
So
what.
C
A
As
a
follow-up
to
this
stuff
on
early
life
that
we're
talking
about
I'd
like
to
go
over
a
paper
on
auto
catalytic
sets,
so
this
is
a
paper
from
Stuart
Kaufman,
William,
hordyke
and
Mike
Steele.
These
are
some
pretty
big
names
in
like
complexity,
Theory
and
modeling,
and
this
paper
is
called
Auto
catalytic
sets
arising
in
a
combinatorial
model
of
chemical
Evolution.
So
this
ties
to
the
origin
of
life.
This
is
talking
about
chemical
evolution
in
the
origin
of
life.
A
A
You
have
chemicals
in
the
environment
of
an
early
Planet,
this
case
early
Earth.
How
did
they
come
together
to
build
coherent
and
self-reproducing
collectives?
And
so
that's
the
question
they're
answering
here.
One
possible
answer
was
proposed
in
the
form
of
emergence
of
an
auto
catalytic,
set,
a
collection
of
molecules
that
mutually
catalyze
each
other's
formation.
That
is
self-sustaining
and
gives
some
basic
food
source.
A
So
you
need
a
couple
of
things
you
need.
One
is
that
Mutual
catalyzation,
because
you
can't
have
a
master
catalyzer
when
a
system
is
self-organizing
and
something
that's
self-sustaining
through
some
sort
of
food
source.
So
there's
got
to
be
some
sort
of
metabolic
input
building
on
previous
work.
Here
we
investigate
in
more
detail
when
and
how
Auto
catalytic
sets
can
arise
in
this
simple
model
of
chemical
evolution,
so
they're
doing
this
modeling
exercise
to
show
how
these
might
arise.
B
A
Catalysis
assignments:
this
is
just
kind
of
a
Innovation
model
that
they
use.
We
derive
theoretical
results.
We
compare
them
with
computer
simulations,
so
this
is
a
lot
of
these
early
life.
Experiments
using
chemical
Evolution
were
done
by
little
parent
and
holding.
Of
course.
These
two
people
are
very
important
in
the
early
in
in
the
origin
of
life
in
an
evolutionary
biology,
so
that
they've,
you
know
these
are
Big
names
in
those
areas.
There's.
A
Be
plausible
through
experiments
of
Miller,
so
this
is
from
Miller
urray
the
Miller
array
experiments
recently
different
variants
of
these
experiments
were
repeated
and.
A
Four
is
I
hope
you
get
all
right
there
we
go
yeah,
so
the
number
citation
number
four
is
chemical
analysis
of.
A
Complex
Prebiotic
broth,
part
one
and
then
five
is
this
part:
two
gas,
oil
and
water
in
the
oil
water
interface
so
years
ago
they
did
these
experiments.
These
are
the
Miller
area,
experiments,
production.
A
Acids
under
possible
primitive
Earth
conditions
where
they
took
a
broth
of
different
molecules,
they
put
an
electric
charge
across
them
and
they
produced
a
lot
of
different
metabolites
and
they
redid
the
experiments
more
recently
back
in
2015,
actually
a
little
bit
earlier
than
that,
and
they
found
that
they
got
a
much
richer
array
of
of
biomolecules
to
result
from
it.
So
the.
A
C
A
It's
just
something
to
think
about
we're
thinking
about
early
life.
This
paper
actually
goes
through
a
number
of
different
computational
models
or
theoretical
models
for
understanding
this
citizen
experimental.
The
first
method
is
the
tap
model.
The
tap
model
was
based
on
the
idea
of
combinatorial
innovation,
which
is
where
you
have
a
number
of
different
combinations
that
can
be
formed,
and
this
leads
to
innovation
in
certain
ways.
So
if
you
recombine
things
over
and
over,
you
get
innovations
that
emerge,
and
so
they
use
this
equation
here.
A
Where
m
m
sub
T
is
the
number
of
different
things
at
time.
T
and
Alpha.
Sub
I
is
the
decreasing
sequence
of
probabilities.
So
this
is
again
with
this
stuff,
where
we
talk
about
regenerating
a
bunch
of
model,
a
bunch
of
configurations
of
different
probabilities,
this
this
combinatorial
model,
the
tap
model
actually
probably
would
do
well
to
describe
what
we're
trying
to
do
with
the
Brandenburg
vehicles
and
so
interpret
a
new
context
to
chemical
evolution.
New
molecular
species
are
produced
their
chemical
reactions
of
arbitrary
combinations
of.
B
A
Is
exactly
the
kind
of
thing
that
happened
in
the
military
experiment,
except
it
happened
in
great
parallelism
and
you
know
you
get.
You
have
a
basically
a
huge
broth
of
possibilities
there
now
this
above
equation,
this
m
sub,
t
plus
one
and
solving
for
that-
represents
a
deterministic
version
that
does
not
guarantee
M
sub
T
to
be
an
integer
value
and.
A
The
general
idea
behind
the
model,
so
these
are
stochastic
implementation
for
their
simulations
here
for
each
newly
created
molecular
species
X
in
each
of
the
existing
molecule
types
y
that
were
not
present
at
Time
Zero
at
scheme
catalyze
the
formation
of
Y
with
a
fixed
probability
P.
Similarly,
for
each
chemical
reaction,
r
that
produces
a
new
species
and
each
of
the
existing
molecule
times
y
that
were
not
present
at
Time
Zero
y
can
catalyze
R,
also
with
probability
P.
These.
B
A
Through-
and
they
do
this-
that
there's
an
algorithm
tapped
with
catalysis,
they
give
the
algorithm.
This
is
pseudocode.
It
basically
describes
this
process,
then,
over
time,
the
M
sub
T
existing
molecular
species
in
the
particular
chemical
reactions
and
produce
them
thus
form
a
growing
chemical
reaction,
Network,
which
is
shown
here,
there's
a
food
set
containing
of
consisting
of
the
M
suppose
initial
species,
as.
A
Here
so
this
is
where
you
have
random.
A
Assignments
and
the
dashed
arrows
and
this
feed
forward
network
with
the
solid
arrows.
So
this
is
over
time.
This
is
over
M
Sub
0
m
sub,
1
M
sub
2
m
sub.
Three,
you
end
up
at
10.,
so
that's
what
their
Network
looks
like.
They
also
have
RAF,
which
is
now
the
probability
that
such
a
growing
chemical
reaction
Network
and
some
at
some
point,
a
subset
of
molecule
types
exist
in
which
the
molecule
mutually
catalyze,
each
other's
production,
which
is
sustainable
on
the
given
food
set.
So.
A
Is
this
idea
of
reflexively
Auto,
catalytic
and
food
generated
set
graph?
More
formally
graph
is
a
set
of
our
chemical
reactions
and
the
molecule
types
involved
in
them
such
that
number.
One.
Each
reaction
in
R
is
catalyzed
by
at
least
one
of
the
molecules
involved
in
our
and
two
each
molecule
type
involved
in
R
can
be
created
from
the
food
set
through
a
sequence
of
reactions
from
R
itself.
So
then
they
use
a
some
sort
of
algorithm
to
find
such
refsets
in
an
arbitrary
chemical
reaction.
Network
and
we're
determine
the
no
subset
is
present.
A
A
Generated
molecules,
and
is
the
union
of
all
possible
graphs
within
a
given
Network,
so
then
tap
and
wrap
can
be
used
in
tandem.
You
can
look
at
graph
sets
in
the
tap
model,
and
this
is
this
was
done
in
the
context
of
technological
evolution
in
21.,
which
is
this
paper
here.
Dynamics
of
a
birth
death
process
based
on
combinatorial
Innovation,
and
this
is
where
you're
looking
at
the.
A
Death
of
combinatorial
Innovations,
so
you're,
looking
at
like
things
that
innovations
that
die
and
are
born
and
the
process
there
so
you're
you're
getting
you
can
apply
this
model
to
other
things
other
than
the
origin
of
life.
But
in
this
case
they
apply
to
the
origin
of
life
and
they
do
a
lot
of
modeling
here
for
different
parameter
values
and
show
that
this
model
is
fairly
effective
at
doing
what
they
want
to
do.
A
A
A
C
A
Yeah
or
if
there's
one
wheel,
you
know
I
mean
it's
really
about.
Like
figuring
out,
you
know
what
what
the
structure
you
know,
what
what
function
is
because
function
can
be.
You
know
kind
of
surprising
if
you're,
just
putting
Parts
together,
okay.
C
You
know
you
could
say:
okay
if
it
can't
move
from
a
spot
like
if
it
goes
around
in
circles.
At
one
point,
then,
obviously,
it's
not
viable
in
the
sense
that
it
couldn't
get
any
food
right.
C
Okay,
that
would
be
an
example,
so
the
distance
it
can
move
per
unit
time
might
be
a
Criterion
for
how
much
its
function
is
working
right.
C
A
Think
a
lot
of
that
was
robotics
because
they're
interested
in
like
how
a
robot
might
move.
If
you
add
or
subtract
Parts,
you
know
if
maybe
there's
something,
that's
very
optimal.
If
you
have
a
weird
morphology,
you
know
like.
C
Yeah,
so
that's
a
possibility
and
I
know:
there's
some
sort
of
self-repairing
and
there
were
robustness,
is
supposedly.
B
Yeah
there
was
the
a
program
that
looked
at
tensegrities
and
they
kept
taking
out
the
struts
that
weren't
necessary
because
they
weren't
weren't
being
used
or
didn't
have
any
pressures.
B
It
started
off
kind
of
square
or
what
you'd
call
pointy
and
then
it
gradually
rounded
became
a
more
rounded
structure.
So
I
love
that
paper.
Yes,
very
interesting,.
B
C
You
know
the
I'm
trying
to
thank
the
we
there's
an
analogy,
so
I've
been
looking
at
the
minimal
self
right
and
the
way
they
make
a
mineral
cells.
They
take
a
very
small
cell
and
they
keep
removing
stuff
right,
maybe
invite
mutations
or
whatnot,
and
they
they
got
them
down
to
only
70
000
Parts.
But.
C
B
C
C
Okay,
so
I
think
they
got
this
thing
both
for
metabolizing
and
self-dividing
and
both
in
the
living
cell-
and
it
was
computer
simulation
of
it.
A
C
C
A
B
A
I
think
this
is
what
you're
talking
about
this
is
actually
I.
Think
you
sent
me
this
copy,
but
I
I
saw
it
talk
on
this
at
a
conference
this
summer.
This
person
is
at
the
University
of
Illinois
and.
A
And
they
they
did
a
they
did
this
at
a
conference.
This
summer
we
talked
about
it
and
they're
doing
this
stuff,
with
This
Is
Fundamental
behaviors
emerging
simulations
of
a
living
minimal
cell.
So
this
is
where
you're
building
a
minimal
cell
you're,
taking
out
like
everything
that
doesn't
isn't
required
for
the
cell
dysfunction
and
then
trying
to
build
a
cell
that
has
like
the
bare
components.
A
So
the
oftentimes
like
in
bacterial
cells,
will
take
out
all
the
genes
that
aren't
essential
and
they'll
have
this
list
of
essential
genes,
and
you
might
want
to
do
that
say
to
like,
if
you
want
to
build
a
bacterial
cell,
that
can
just
function,
metabolically
and
then
booted
up
with
genes
to
do
something
like
you
know,
some
some
task
that
they
want
the
cell
to
do
so,
that's
why
you
might
want
a
minimal
cell.
This
is
the
basic
metabolic
requirements
of
a
cell
without
any
other
function
really.
A
C
C
A
C
C
A
A
Yeah
yeah,
then
they
have
these
receptors
here
and
ribosomes.
So
they're
like
they're,
looking
at
kinetic
data
from
experiments,
they're
going
to
get
cellular
processes,
then
when
they
get
that,
like
they
have
the
biological
side,
then
they
build
these
whole
cell
simulations,
which
are
these
dynamical
systems
that
predict
the
cell,
what
the
cell
does
and
then
they
they
compare
it
with
the
biology.
So
you
get
a
good
comparison
of
a
simulation
with
the
biology,
so
their
simulations
are
highly
detailed
and
highly.
You
know
like
they.
A
From
the
bio
biology
of
the
simulation
yeah,
so
they
do
this
GP,
they
run
it
on
a
GPU,
the
simulation
and
it's
you
know,
they're
able
to
extract
different
parameters.
So
these
time
dependent
cell
States,
looking
at
mRNA
cell
doubling
time
and
ATP
cost
so
yeah
so
yeah.
This
is
a
3D
spatial
resolution
of
a
fully
dynamical
wholesale
kinetic
model.
A
Then
you
have
these
single
reactions
that
are
pretty
detailed.
You
have
time
these
time
dependent
cell
State
measurements,
which
are
of
course
this
function.
Here
you
have
I
talked
about
mRNA
half-lives
and
looking
at
like
a
process
where
you
know,
if
you
have
a
transcriptional
process,
you
can
look
at
the
MRNA
half-life
of
that
process.
So
if
something
is
transcribed,
you
know
how
long
does
the
MRNA
live
in
the
cell
and
I've
done?
A
Experiments
like
this,
where
you
can
shut
off
the
mechanism
and
see
what
the
MRNA
Half-Life
is,
and
it
tells
you
something
about
the
underlying
mechanisms
of
metabolism
and
then
connections
among
metabolism.
Genetic
information
and
cell
growth
are
revealed,
so
they
actually
can
do
a
lot
of
these,
not
just
like
looking
at
a
minimal
genome.
It's
looking
at
the
whole
cell
and
how
it's
behaving
so
yeah,
let's
see
so
they
have
this
whole
cell,
fully
dynamical
kinetic
model
which
they
call
wcm
wholesale
model
of
jcbi
sim3a,
which
is
this
minimal
cell.
A
And
that's
like
a
you
know
again:
it
has
a
reduced
Genome
of
493
genes.
So.
A
So
this
is
where
they're
not
interested
in,
like
the
regular
functional
regulation,
they're
interested
in
just
kind
of
like
the
essential
metabolic
genes,
they're
doing
cryo-electron
topographs
to
to
get
sort
of
the
image
of
the
cell,
so
they're
Imaging
the
cell,
so
that
they
can
put
it
in
put
it
into
a
computational
model
of
the
cell
geometry,
ribosome
distributions
time,
dependent,
behaviors
of
concentrations
and
reaction,
fluxes
from
a
stochastic
deterministic
simulation,
so
they're
doing
different
types
of
concentration
and
reaction,
flux,
simulations
that
involves
a
lot
of
flux,
balance,
analysis
and
all
that
fun
stuff.
A
So
that's
not
that's
not
trivial.
It
requires
a
lot
of
computational
power,
but
that's
part
of
the
simulation
as
well.
This
reveals
how
the
cell
balances
demands.
The
cell
balances
demands
of
its
metabolism,
genetic
information
processes
and
growth.
So
there's
this
they
want
to
see
how
these
things
are.
A
You
know
basically
what
the
cell
is
investing
in
each
of
these
things
and
offers
insights
into
the
principles
of
life
for
this
minimal
cell.
The
energy
economy
of
each
process,
including
active
transport
of
amino
acids,
nucleosides
and
ions,
is
analyzed.
Wcm
reveals
how
emerging
imbalances
lead
the
slowdowns
and
the
rate
of
transcription
and
translation.
A
A
When
you
have
transcription
you're
measuring
it
from
the
production
of
mrnas,
you
can
watch
the
sort
of
the
concentration
of
those
and
you
know
for
in
terms
of
slowdowns.
The
mrnas
have
a
certain
Half-Life,
so
they
survive
in
the
cell
and
if
the
number
of
our
marinas
Falls
the
concentration
of
them
Falls,
and
you
can
assume
that
that
function
has
been
shut
down
or
diminished
in
some
way.
And
if
it's
you
know,
if
there's,
if
there's
a
higher
concentration
of
mrnas,
you
assume
that
that
process
is
enhanced.
A
A
A
So
these
are
all
things
that
the
you're
just
looking
in
the
experimental
system
and
you're
using
micro
mycoplasmas
in
this
case
in
this
paper-
and
so
this
is
a
very
simple
cell-
and
you
know
it's
very
easy
to
manipulate
and
to
observe.
So
that's
that's
why
they
use
micro,
mycoplasma,
and
so
we
have
been.
We
have
been
able
to
produce
living
cells
with
fewer
genes
than
any
known,
naturally
occurring,
so
so
this
is
some
of
their
work.
A
A
A
lot
of
this
involves
like
not
just
like
looking
at
certain
measures,
but
doing
a
lot
of
flux,
balance
analysis,
which
is
really
kind
of
a
difficult
thing
to
get
your
head
around
how
it
works,
because
there
are
these
really
huge
networks
that
are
have
a
lot
of
feedbacks.
A
Let's
see
this,
this
jcvi
Sim
3A
is
a
genetically
minimal
bacterial
cell,
consisting
of
only
493
genes
on
a
single
543
kilobase
pair
of
circular
chromosome.
So
that's
about
that's
a
pretty
small
chromosome
like
compared
to
you
know
like
the
human
genome
or
even.
B
A
Animal
genome
circular
and
it's
pretty
much
optimized,
there's
not
a
lot
of
right
there,
very
little
regulatory
or
extraneous
DNA
in
that
in
that
Circle
and
where
they
have
452
genes
coding
for
proteins.
C
A
B
A
Gram-Positive
bacteria
mycoplasma
liquidys,
subspecies
Capri,
it's
a
certain
strain
here
dm12
and
has
been
synthetically
reduced
to
achieve
a
minimal
genome
producing
living
cells
like
row,
divide
it,
grow
and
divide
in
about
100
minutes
and
have
consistent
spherical
morphologies
with
400
to
500
nanometer
diameters.
A
So
this
is
the
size
of
the
cell,
their
their
genetics
are
such
that
they
divide
in
about
100
minutes,
and
then
they
have
these
spherical
morphologies,
which
are
actually
pretty
small
cells.
So
that's
that's.
B
A
Kind
of
thing
we're
dealing
with
here,
in
addition
to
biochemical
reactions,
I,
will
sell
3D
spatial
models
require
a
cellular
architecture,
including
spatial
distributions
or
ribosomes
configurations
of
the
circular
chromosome.
B
A
Of
diffusion
is,
it
increases,
makes
the
spatial
distribution
less
important.
The
cellular
architecture
is
a
reconstructed
at
the
Single
Cell
level,
directly
from
cryoelectron
tomographs.
A
A
So
that
they
can
actually
kind
of
replicate
the
the
inside
of
the
cell
and
some
of
these
things
so
see
if
we
go
here
to
this
part.
C
B
A
B
A
A
different
you
know
different
setups,
whereas
so
these
are
chemical,
Master
equation,
they
work
from
that
and
so
a
lot
of
times.
You
will
assume
that
the
cell
is
well
stirred
and
you
know
it
includes
diffusion
and
rates
of
transcription,
and
so
it
has
all
these
different
rates
involved
in
it,
but
it
doesn't
require
any
sort
of
spatial
segregation
of
mechanisms.
It's
all
everywhere
in
the
cell
has
an
equal
chance
of
this.
These
parameters
being
correct,
and
so
that's
why
they
say
well
stirred
and
then
a
reaction,
diffusion,
Master,
equation
description.
A
They
requires
macromolecules
that
diffuse
to
each
other
for
reactions
that
take
place
in
the
spatial
heterogeneous
environment
of
the
cell.
So
they
assume
that
these
rates
are
constant,
but
that
they're
these
diffuse,
these
macromolecules
of
diffuse
and
they
interact
in
different
parts
of
the
cell.
A
A
C
The
spatial
model
was
that
yeah,
that's
what
see
there's
an
interesting
parameter,
so
I
got
84
percent
of
the
simulated
cells
persist
in
the
sense
of
at
least
for
the
number
of
Cycles
like
that
or
are
those
would
still
be
classified
as
a
lot
yeah
yeah,
okay,
so
only
16
percent
were
terminal.
C
A
C
A
C
C
If
it's
greater
than
zero
percent,
then
there's
a
mutation
mechanism
and
major
Evolution
and
start
getting
better.
C
But
you
know
what
we
could
use
from
him
is
a
clear
statement
of
what
is
the
difference
between
his
approach
and
inverse
and
why
he's
so
down
on
Amber.
B
C
B
Yes
and
Stephen
Levin
says
that
even
the
struts
and
the
strings
of
your
model
are
also
a
tensegrity
structure,
which
is
what
they
are.
If
you
look
at
actin,
it's
an
Integrity
start,
oh
okay,
so
you
have
to
put
that
in
there
as
well.
In
other
words,
it's.
C
Okay,
so
yeah
I
think
the
problem
is
to
get
Beyond
anger,
but
be
careful
what
you
take
from
beloved.
B
C
B
Yeah
so
I
think
I
should
try
to
produce
that
for
the
struts
and
strings
of
my
model
and
then
just
like
I
say
call
them
today:
okay
and
see
the
difference
between
linear
and
not
and
and
say,
researchers
and
and
then
say
whether
my
measurements
with
this
are
going
to
be
better
than
the
just
the
Continuum
model,
and
that's
all
I
have
to
do
is
just
say:
does
this
model
here
work
better
than
the
continental
mod
who
wants
more
computationally
intensive.
C
For
my
project,
okay,
Bradley
getting
back
to
that
paper,
then
all
right-
the
questions
I've
got
are.
C
C
Let's
see,
in
other
words,
are
they
essentially
the
same
or
not
one
road
slower
than
the
other
way
results?
The.
A
Same
let's
see
if
they're
they
have
any
figures
that
explain
that
I,
don't.
B
C
A
B
Reactions
in
microgravity
have
a
different
timing.
They've
automatically
have
a
different
different
time
sequence.
So
that's
a
molecular
level
thing.
Yeah.
C
B
I
would
like
to
see
that
to
see
how
important
it
is
at
that
size
would
be
interesting.
C
A
I,
don't
think
so
they
just
mentioned
that
things
are
either
well
mixed
or
not,
and
a
lot
of
this
might
be
because
you
have
you
know
hydrophobicity
of
DNA
and
at
that
scale
it's
like
that's
really
kind
of,
because
it's
pretty
packed
in
as
you
see
from
the
sea.
So
this
is.
This
is
the
cell.
This
is
the
model
of
the
cell
here,
so
we
have
this
Digital
model
of
the
cell.
This
is
the
image
or
we're
taking
these
coordinates
from
the
image
and
then
we're
building
this
model.
A
And
then
this
is
what
we're
simulating.
So
you
get
like
these
macromolecules
that
are
maybe
clustered
or
not
you're
moving
around
and
they
can
interact.
You
know
they
can
have
a
do
some
reaction
anywhere
in
the
in
the
cell,
which
is
of
course
very
small,
and
then
they
through
the
spatial
simulations
they
do
I,
don't
know
if
they
really
break
it
out.
I,
don't
know
if
they're,
comparing
the
two
well-mixed
and
spatial
that
might
be
further
down.
C
A
I
think
everything
is
a
coordinate.
It's
just
that,
like
the
spatial
model
assumes
that
there's
like
like
I
guess,
maybe
compartmentalization
almost.
A
C
And
okay,
now
the
Curious
thing
is
I
I,
looked
up,
the
rates
of
diffusion
in
crowded
cells,
okay
and
the
fusion
rate
same
for
macro
molecules
to
go
down
only
by
a
factor
of
two
or
three,
so
they
may
slow
things
down
a
little
bit,
but
I
suspect
that
crowded
chronic
Behavior
does
not
make
much
of
a
difference.
A
That's
interesting.
So,
let's
see
if
there's
anything
on
this
is
comparisons.
A
They
have
some
supplemental
figures
which
I'll
get
to
in
a
minute
here.
A
Gene
expression
between
will
stirred
and
spatially
resolved
simulations,
so
I
guess
the
spatially
resolved
is
where
they
have
the
coordinate
information
so
that
they
know
where
and
then
so.
They
just
have
accounts
for
RNA
mRNA
for
genes
coding
for
genetic
information
processing
proteins
over
time.
This
is
the
MRNA
count.
This
is
the
time,
so
you
can
see
that
there's
in
the
spatial
resolved.
B
A
Yeah,
you
have
more
sort
of
it's
it.
It
fluctuates
more
I
guess
over
time,
that
could
just
be
an
artifact
of
having
a
spatial
information
there,
as
opposed
to
the
well
stirred
where
you
have
just
a
count,
basically
yeah.
A
Are
being
incorporated
into
mRNA
in
the
I
guess
in
well
stirred
model
and
then
second,
the
current
spatial
model
does
not
include
DNA
replication,
which
initiates
on
average
around
10
minutes
in
the
well
Stern
model.
So
this
is
yeah.
It
still
doesn't
really
give
a
lot
of
insight
into
that
difference.
So.
C
So
on
the
parameters
that
could
measure
the
spatially
resolved
is
about
the
same
as
well:
Stern
yeah.
A
A
C
C
So
this
is
yeah.
We.
A
I
don't
know
if
that
would
give
us
any
more
insight
into
that.
Let's
see
yeah.
B
B
B
A
Set
is
the
concentration
of
intracellular
pools
of
NDP
ntp
and
ADP,
so
these
are
macromolecules,
and
you
can
see
that
there's
a
difference
here.
The
spatial
spatial
result
room
again
has
more
variation
and
fluctuation
the
scale
protein
counts.
These
are
a
number
of
unique
proteins.
There's
a
much
difference
there
and
then
the
number
of
unique
mrnas
are
the
this.
The
accounts
for
the
half-life
in
minutes.
A
So
this
is
just
things
that
are
getting
synthesized
and
degrading,
so
you
get
more
more
unique
mrnas
in
the
spatial
resolved
model,
but
it
decays
a
little
bit
faster.
At
least
you
know,
according
to
this
histogram
and
see
so
in
terms
of
our
mRNA
Half-Life
they're,
compared
between
the
two
methods,
where
the
well-stirred
half-lives
depend
on
the
act
of
the
greatest
sum
statistics
in
the
spatial
model.
So
this
is
something
that
there's
a
linkage
here
between
the
two.
A
The
well
stirred
model
is
longer
half-lives
on
average
than
the
half-lives
in
the
spatial
model,
as
we
see
here,
and
they
don't
really
see
why
that
is
exactly.
But
but
there
is
also
agreement
between
the
Wall,
Street
and
spatial
simulations
and
the
MRNA
comes
in.
The
spatial
model
are
higher,
in
average,
likely
due
to
the
difference
in
transcription
rates
between
the
two
models.
So
it's
the
spatial
model
also
has
lower
concentrations
the
nucleotides,
and
then
we
talked
about
that
so
yeah.
There's
there's
a
lot
of
like.
A
A
Okay,
yeah,
okay,
so
yeah
Jesse
was
here
well
thanks,
Jesse
for
attending
for
a
period
that
you
did
so
do
we
have
anything
else
to
say
about
that
paper.
I
was
big
picture.
C
Okay
so
basically
the
idea
that
diffusion
is
sufficient
to
move
things
around
yeah
same
drought,
then
some
of
the
the
non-special
model
may
be
adequate
right.
A
A
A
In
another
paper,
yeah
I
think
their
focus
here
was
on
some
of
the
internal
mechanisms
of
the
cell.
What's
going
on
there
because.
A
C
C
A
C
A
A
A
C
B
Okay,
it's
a
now
I
may
say
the
skeletons
there's
a
lot
of
literature.
B
B
Notes,
no,
that's
not
it.
Oh,
oh,
it
went
somewhere
else.
B
Anyway,
I'm
sure
they
included
it
in
my
course
on
Cell
cytoskeleton,
so.
A
Yeah,
that's
okay,
yeah
well,
I
think
that
was
yeah.
That
was
a
really
good
paper
for
understanding
how
people
are
simulating
cells
and
having
the
parts
there
in
a
very
simple
cell
that
would
describe
sort
of
a
function
in
a
cell
and
what
you
need
there
and
how
those
things
behave.
So
I
mean
Indians,
larger
insights.
I
know.
The
whole
point
of
this
is
to
look.
C
Thank
you.
There's
anyone
invited
Melvin
to
give
us
a
talk.
A
Steve
Levin
yeah,
yeah,
I
guess
so:
I
haven't
gotten
around.
B
Well,
Stephen
M11,
he
sent
me
an
email,
so
I
could
send
you
his
email.
A
B
Don't
know
anyway,
the
emails
are
are
about
10
segregate
and
he
has
been
following
some
Vivo
wormpings
that
he
dropped
in
on
a
session
from
one
point.
A
A
Work
from
what
was
it,
the
embryo
Physics
course
that
was
the.