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- The
anaphase-promo
ting complex:
proteolysis in
mitosis and
beyond.: Mol Cell, Vol.
9, No. 5. (May
2002), pp.
931-943.Key
events in
mitosis such
as sister
chromatid
separation and
subsequent
inactivation
of
cyclin-depende
nt kinase 1
are regulated
by
ubiquitin-depe
ndent
proteolysis.
These events
are mediated
by the
anaphase-promo
ting complex
(APC), a cell
cycle-regulate
d ubiquitin
ligase that
assembles
multiubiquitin
chains on
regulatory
proteins such
as securin and
cyclins and
thereby
targets them
for
destruction by
the 26S
proteasome.JM
Peters
Source: Mol Cell, Vol. 9, No. 5. (May 2002), pp. 931-943. - Structural and
numerical
chromosome
changes in
colon cancer
develop
through
telomere-media
ted anaphase
bridges, not
through
mitotic
multipolarity.: Proceedings of
the National
Academy of
Sciences of
the United
States of
America, Vol.
102, No. 15.
(12 April
2005), pp.
5541-5546.Telo
mere
dysfunction
has been
associated
with
chromosomal
instability in
colorectal
carcinoma, but
the
consequences
of
telomere-depen
dent
instability
for chromosome
integrity and
clonal
evolution have
been little
explored. We
show here that
abnormally
short
telomeres lead
to a wide
spectrum of
mitotic
disturbances
in colorectal
cancer cell
lines,
including
anaphase
bridging,
whole-chromoso
me lagging,
and mitotic
multipolarity.
These
abnormalities
were found in
both the
presence and
absence of
microsatellite
instability.
The mean
telomere
length varied
extensively
between cells
from the same
tumor,
allowing the
establishment
of tumor cell
subpopulations
with highly
different
frequencies of
mitotic
disturbances.
Anaphase
bridging
typically
resulted in
either
inter-centrome
ric chromatin
fragmentation
or centromere
detachment,
leading to
pericentromeri
c chromosome
rearrangements
and loss of
whole
chromosomes,
respectively.
There was a
strong
correlation
between
anaphase
bridges and
multipolar
mitoses, and
the induction
of dicentric
chromosomes by
gamma
irradiation
and telomerase
inhibition led
to an elevated
frequency of
multipolar
mitotic
spindles,
suggesting
that
multipolarity
could result
from
polyploidizati
on triggered
by anaphase
bridging.
Chromatid
segregation in
multipolar
mitoses was
close to
random,
resulting in
frequent
nullisomies
and nonviable
daughter
cells. In
contrast,
there was a
high
clonogenic
survival among
cells having
gone through
anaphase
bridging in
bipolar
mitoses.
Bridging of
telomere-defic
ient
chromosomes
could thus be
a major
mutational
mechanism in
colorectal
cancer,
whereas
mitotic
multipolarity
appears to be
a secondary
phenomenon
that rarely,
if ever,
contributes to
clonal
evolution.Y
Stewénius, L
Gorunova, T
Jonson, N
Larsson, M
Höglund, N
Mandahl, F
Mertens, F
Mitelman, D
Gisselsson
Source: Proceedings of the National Academy of Sciences of the United States of America, Vol. 102, No. 15. (12 April 2005), pp. 5541-5546.
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