and the disintegrated debris, each
enclosed in cell membranes, are consumed by phagocytes (“cell eaters”).
It is estimated, for example, that
phagocytes consume 1011 blood cells
a day. Other cells experience necrosis,
which is triggered from outside the
cell causing the cell to rupture and
spew its contents into intercellular
space. One way this can happen is if
cells have experienced some form
of trauma. Viruses can invade cells,
commandeer the DNA interpretation
system (that is, ribosomes) with their
own DNA, and eventually rupture the
cell wall, broadcasting new virus particles into the surrounding tissues.
Once a cell has stopped replicating,
it may not immediately experience either apoptosis or necrosis. Rather, it
may continue to exist in a senescent
state, which I have chosen to label
an increasingly grumpy state. It may
continue to produce proteins but they
may prove to be harmful to other cells.
The aging process and its manifest
side effects can be traced, in part, to
grumpy old cells spewing harmful
products into the biological neighborhood. One thinks of the plaques and
tangles of Alzheimer’s disease and
the misfolded prions associated with
caused by harmful proteins synthesized by grumpy cells.
If you got all the way to the end
of this column, congratulations! No
matter how complicated we think our
software systems have become, we can
still marvel at the extraordinary complexity of the life of a single cell and
the immeasurable complexity of multicellular life, including our own.
Vinton G. Cerf is vice president and Chief Internet Evangelist
at Google. He served as ACM president from 2012–2014.
Copyright held by author.
I AM GOING way out on a limb in this column into an area where I really know very little but am completely fascinated by what I am learning. The tenuous
linkage to our discipline is what I will
call programmed cell self-destruction or
maybe cell suicide.
I have been reading at length a
book called Molecular Biology of the
Cell. This is a 1,342-page book, not
counting index and glossary and a
separate book of problems. It is profusely illustrated and eminently readable even by a layperson like me, pretending, of course, that I am actually
understanding what I am reading.
It turns out that cells reproduce
(that is, divide: mitosis) but usually
only a finite number of times. When
they divide, their DNA is duplicated
within the cell and separate copies are
transported into each new daughter
cell. Human DNA comes in 23 distinct
chromosomes. Each chromosome
is made up of a double helix of DNA.
During cell mitosis, each strand of the
double helix is duplicated by figuratively unzipping the double helix and
replicating each strand. The replication takes place at multiple replication
origin sites along the strand so this
process operates in parallel. The now-duplicated chromosomes look like
elongated “X”-shaped Gumby characters formed by adjacent DNA strands.
As the mitotic process continues, the
duplicated chromosomes are pulled
apart by microtubules that attach to
opposite sides of the paired chromosomes. As the process proceeds, eventually two new nuclei form with its
copy of the original cell’s DNA and the
cell completes its division into two essentially identical cells.
At the ends of each strand of
DNA is a repetitive sequence of DNA
called a telomere. There are multiple
telomeres at each end of the chro-
mosome. One might think of them
figuratively as handles needed to an-
chor the DNA during the unzipping
and replication process. The telo-
meres themselves are not replicated
in this process, so every cell division
may lose one or more telomeres. If
there are too few telomeres left, the
replication process fails and initi-
ates a process known as cell apop-
tosis, which we can think of as pro-
grammed cell death. Interestingly,
certain kinds of cells known as em-
bryonic stem (ES) cells found in bone
marrow and in the gut contain an
enzyme called telomerase that fabri-
cates new telomeres so that ES cells
can replicate indefinitely. Non-ES
cells, which make up most cells in
our bodies, count down to termina-
tion of replication. Cancer cells man-
age to avoid this outcome by using
telomerase to make more telomeres
allowing indefinite proliferation.
Cellular apoptosis can be triggered
within the cell or by outside factors
Grumpy Old Cells
DOI: 10.1145/3028774 Vinton G. Cerf
we think our
we can still marvel
at the extraordinary
complexity of the
life of a single cell.