cells do not die in the same way.

it is harder to detect apoptosis than mitosis, due to the later deriving in two
cells in lieu of no-cell like apoptosis.
there are two types of cell death :
Intrinsic or cell autonomous (by the cell itsself)
Etrinsic or cell non autonomous ( death is triggered by other cells or their
microenviroment)
!rogrammed cell death is intentional whereas necrosis is the process which
entails acute in"ury or physical damage so a cell dies.
programmed cell death is neccessaary for multicellular organisms both in
their development and their interactions with the outer world.
!#$ can be used for scuplting: In the uterus, fetus have webs between their
%nger, which are elimanated through !#$.
http:&&www.youtube.com&watch'v()*+,-./lo0E1feature(youtu.be
!#$ can be used to delete structures no longer necessary like mamary
glands2 in seual dimorphism: 3hen the fetus does not possess a gender,
structures like the *4llerian and 3ol5an duct eist to assist in chores related
with ecretion during fetus development. If the fetus turns out to be a female,
then the *4llerian duct becomes the oviduct and thee uterus, along with the
elimination of the wol5an ductt. In males, *4llerian ducts are degenerayed
through !#$, the 3ol5an ducts become the vas deferens and the seminal
vesicles
!#$ is also used to ad"ust the number of cells: In fetuses, there is a vast
ecess of neurons that must be eliminated in order to form the neuronal
circuits and thus, it is also needed as a way of enabling brain functions.
!#$ helps in the process of eliminating harmful agents such as virus or
bacteria: . cells are produced in the .hymus, and the in %rst glance , are
underdeveloped cells. .he only way to test their e6ectiveness is through the
dendritic cells which have self antigens. If a . cell binds strongly to those
antigens, then it must be eliminated through !#$. .he remainders survive
and mature into fully-developed .-cells.
3hen 789 rays hit our epidermis layer, some carbon-polyhydrates aromatic
compunds forms inside the cells which produces a distortion on the $:;. It
can be %ed through % pathways, but if not then !#$ is induced.
3hen !#$ goes south abnnormal developments occur. If there is a high
number of cells deleted through !#$ in neuronal circuits, then normal
fuctioning is no longer posible (i.e hungtington or parkinson)
detrimental-lupus
apoptosis( &;potosis&
#ells separates from the tissue and it neirbhouring cells and shrinks, due to
cytoplasm and chromatine condensation and then fragmentates then are
engulfed by macrophages( !hagocytosis) through lysosomes.
http:&&youtu.be&k;/er<gEnc
#ell death speci%cation- #ommitment to cell death(!=:>)
:ecrosis: #ell swells-rupture of organelles-plasma membrane destroyed.
;poptosis does not realease to intercellular enviroment. :o immune response
contrary to necrosis.
$na frag. happens when crhromatin is cleaved in ?@A bases fragments.
assay they die by frag.
Endonucleases are en0ymes that are activated for cleaving.
!hagocytes recogni0e apoptetic cells
phosphatidylserine(!/) a phospholipid
!/ is inside in helathy cells
asymetry is presentt in apoptotic cells, due to negative charged !/ ( !/
eternali0ation)
;nnein 8 binds to :egative !/, Buorescent microscoping
Clippases is related to !/ Bipping. DeaBet
Eenotype2!henotype
.umorigenesis
/omatic mutation(Everywhere ecept form germ cell, therefore not
transmited to o6spring)
Eerm line(=6spring)
Collicular lymphoma
Dymph :odes %lter foreign particles and are conected to the lymphatic
vessels
tonsils thymus blood marrow.
Dymphoma white cells blood cancer and b and t cells are increased
Collicular lymphoma Increased 9cells that a6ects spleen and lymph nodes
happens a translocation between chromosomes ?F and ?@ by switching lower
arms
G,AAA gens
3hat is a gene'
.ranscription unit is the section of the gene transcribed from dna to rna. It
has the eons which are included in m>:; .
Introns are ecluded.
,,utr and <,utr are not included but important for stability and locali0ation of
the gen
promoter is the 0one where machinery can dock.
Enhancer activates machinery
silencer cis regulatory determines where to stop.
;rm ?F Immunoglobulin heavy chain locus- antibodies
;rm ?@ 9#D-G very high epression of b-cells by translocation due to
enhancer in arm ?F
oncogenes when overepressed produces tumorigenesis.
c-myc is a protooncogene then chromosomal translocation- burkitt
lymphoma.
bcl-G does not promote cell proliferation but apoptosis
growth factors do not promote tumorigenesis in bcl-G, after removing growth
factors cell do not undergo apoptosis.bcl-G blocks apoptosis.
tumors happen in sevreal dna changes
by blockking apoptosis, secondary mutaations can happens.
bcl-G is a proto-oncogene.
bcl-G associates with myytochondria and rough edoplasmatic
mitochondria clacium storaage, Iron-sulfur-synthesis
co-immunoprecipitation
9a is an interactor of bcl-G
9a promotes apoptosis, is a killer protein
ba dominates over bcl-G
ba to bcl-G ratio a6ects apoptosis rates
bcl-G blocks ba activity.
yeast two-hybrid
gene (locus
transcriptional activators formed by activation domain and bind dominain
bait and prey by fussion of dna or activation domain so bcl-G binds to
preys(9ait)
9;$ was found through yeast
can interact with bcl-G but no ba
bh< region is in all proteins bcl-G bad and ba
bad binnds to bcl-G, anntagoni0es bcl-G avoiding ba contact and therefore
apoptosis. 9;$ si a pro-apoptosis protein.
9#D-G superfamiliy
/ensors: !ro-apoptotic : -ydrophobic tail and all bh< domain
no homology to other groups
Euardians: ;nti-apoptotic
have hydrophobic tail and have all F regions
9#D-G 9cl-D
viruses make proteins that act k"e guardiasn
e6ectors dont have bhF domainand have hydrophobic tail
9;H and 9;)
they can form heterodymes
e6ectors because induce apoptosis.
/ensors bind to guatdians and avoid anti-apoptotic like e6ectors
sensors can activate e6ectors
>edundancy of superfamily makes more robust systems
ubi+uitously
9a and bak phenotype arti%cial gain of function
through ba and bak, it was demonstrated that both have redudant functions
because apoptosis is blocked.
3EE) ?: Introduction to apoptosis and 9cl-G superfamily
?.G - 3hat is programmed cell death'
#ell death
!rogrammed cell death
:ecrosis
?.< - -allmarks of apoptosis
!rogrammed cell death type I (apoptosis)
!rogrammed cell death type II (autophagic cell death)
!yknotic nuclei
!hagocytosis (engulfment)
!hagocytes
*acrophages
Dysosomes
$:; ladder (nucleosomal ladder)
.7:ED assay
Endonucleases
!hosphatidyl serine
Eat-me signal
!/ eternali0ation
;nnein 8
Clippases
?.F - .he 9cl-G story
/omatic mutation
Eerm line mutation
Collicular lymphoma
Eene (locus)
.ranscription unit
!romoter
cis-acting regulatory regions
#hromosomal translocation
9cl-G
!roto-oncogene
=ncogene
?., - 9a and 9ad
*itochondria
#o-immunoprecipitations
9a
!ro-apoptotic
;nti-apoptotic
Ieast two-hybrid system
.ranscriptional activator
9ad
?.J - .he 9cl-G superfamily
9cl-G superfamily
/ensors (in the contet of 9cl-G superfamily)
Euardians (in the contet of 9cl-G superfamily)
E6ectors (in the contet of 9cl-G superfamily)
>edundancy