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BEGIN:VEVENT
SUMMARY:Prof. Dr. Oliver Bell (University of Southern California)
DTSTART:20200728T160000Z
DTEND:20200728T170000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/1
DESCRIPTION:Title: How cell fate decisions are maintained by Polycomb\nby Prof. Dr. Oliv
er Bell (University of Southern California) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nTranscriptional silencing
by Polycomb group (PcG) proteins is a major paradigm for epigenetic inher
itance from fly to human. The Polycomb Repressive Complexes PRC1 and PRC2
catalyse distinct chromatin modifications to enforce gene silencing. Howev
er\, the mechanisms underlying the inheritence of transcriptional silencin
g by different PRC complexes are not known. Addressing this question has b
een extremely challenging due to technical limitations that do not discern
the initiation from sequence-independent maintenance of repression. We ha
ve solved this problem by developing an approach to reversibly recruit PRC
1 or PRC2 to transcriptionally inactive or active chromatin in mouse embry
onic stem cells. For the first time\, we directly and systematically inter
rogate the ability of different PcG complexes to (1) form repressive chrom
atin structure\, (2) initiate gene silencing\, and (3) maintain silencing.
I will present an unexpected division of labour between different PRC1 an
d PRC2 complexes in epigenetic silencing.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/1/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Susan Gasser (Freidrich Miescher Institute for Biomedica
l Research)
DTSTART:20200827T080000Z
DTEND:20200827T100000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/2
DESCRIPTION:Title: How and where to assemble heterochromatin\, and why it is essential for o
rganismal survival\nby Prof. Dr. Susan Gasser (Freidrich Miescher Inst
itute for Biomedical Research) as part of Colloquium zooming Molecular & C
ellular Biology LUMS\n\n\nAbstract\nThe establishment and maintenance of c
hromatin domains shape the epigenetic memory of a cell\, with histone H3 l
ysine 9 methylation (H3K(me) defining repressed heterochromatin. In C. ele
gans\, SET-25 (SUV39/g9a) catalyzes to its targets. One requires recogniti
on of MET-2-mediated H3K9me2 by the MBT-domain protein LIN-61. The second
depends on a somatic Argonaut NRDE-3 and 22nt siRNAs. This MET-2-independe
nt pathway makes up ~10% of SET-25 target sequences\, and most notably inc
ludes intact transposons. Compared to single mutants\, met-2\;nrde-3 doubl
e mutant enhances transposon transcription and embryonic lethality. Wherea
s the targeting of SET-25 silences transposons\, whose expression compromi
ses development\, the targeting of MET-2/SET-DB1 is necessary to prevent t
he promiscuous transcription of simple repeats. Simple repeat transcripts
lead to R-loops and fork-associated damage\, that requires BRCA1 to ensure
survival. While the genome becomes unstable\, met-2 mutants show nearly n
ormal developmental and differentiation patterns.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/2/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Dr. Stefan Schoenfelder (Babraham Institute\, Cambridge)
DTSTART:20200911T100000Z
DTEND:20200911T120000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/3
DESCRIPTION:Title: Functional Organization of the Genome in 3D\nby Dr. Stefan Schoenfeld
er (Babraham Institute\, Cambridge) as part of Colloquium zooming Molecula
r & Cellular Biology LUMS\n\n\nAbstract\nThe three-dimensional organisatio
n of the genome is tightly linked to its function. The cell-type specific
folding of the DNA enables gene regulatory elements\, including promoters
and enhancers\, to interact\, in some cases bridging distances of hundreds
of kilobases. These enhancer-promoter contacts are thought to be crucial
for gene expression control. I will discuss recent progress in the methodo
logy to map the 3D organisation of chromatin in mammalian nuclei genome-wi
de\, illustrate on examples how enhancer-promoter contacts dynamically res
pond to signalling cues and are rewired during cell fate transitions\, and
highlight some of the major challenges and open questions in the field.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/3/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Peter Becker (LMU Munich)
DTSTART:20201009T070000Z
DTEND:20201009T090000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/4
DESCRIPTION:Title: Genetic & Epigenetic Mechanisms of X Chromosome Activation in Drosophila<
/a>\nby Prof. Dr. Peter Becker (LMU Munich) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe process of X-chromoso
me dosage compensation in Drosophila involves boosting the transcription o
f most genes on the X in male flies to match the transcription output of t
he two X chromosomes in females. Activation is achieved through histone ac
etylation of active gene chromatin by the histone acetyltransferase MOF. M
OF is recruited to its targets by the dosage compensation complex (DCC). A
ccording to the prevalent model this involves genetic and epigenetic princ
iples: the DCC first binds to a defined number of DNA sequence elements\,
the High Affinity Sites (HAS)\, which are exclusive to the X. The activat
or then identifies and acetylates active gene chromatin in the nuclear nei
ghborhood\, presumably through their epigenetic H3K36me3 signature.\n\nDos
age compensation happens gradually during early embryonic development and
matures along with refined chromosome folding. Key to successful dosage co
mpensation is the property of the DCC to selectively bind the X chromosome
. We continue to explore the molecular principles that allow such selectiv
e regulation. Most recently\, we made significant progress in identifying
and testing such principles by whole-genome chromatin reconstitution in a
cell-free system.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/4/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Sandra Hake (JLU Giessen)
DTSTART:20201016T070000Z
DTEND:20201016T090000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/5
DESCRIPTION:Title: Histones: How much variation do we need?\nby Prof. Dr. Sandra Hake (J
LU Giessen) as part of Colloquium zooming Molecular & Cellular Biology LUM
S\n\n\nAbstract\nAll eukaryotes organize their DNA together with histones
and non-histone proteins into a highly complex nucleoprotein structure cal
led chromatin\, with the nucleosome as its monomeric subunit. Several inte
rconnected mechanisms have evolved to regulate DNA accessibility\, includi
ng nucleosome replacement of canonical histones with specialized histone v
ariants. Deposition of histone variants can lead to profound chromatin str
ucture alterations thereby influencing a multitude of biological processes
ranging from transcriptional regulation to genome stability. At the focus
of our research is the evolutionary highly conserved histone variant H2A.
Z\, which has been extensively studied and shown to play a role in gene ex
pression\, DNA repair\, heterochromatin formation\, chromosome segregation
and mitosis. But the mechanism(s) of how H2A.Z controls these diverse bio
logical processes is not understood. Using state-of-the-art biochemical\,
cell biological\, genome-wide and bioinformatics approaches we are sheddin
g light on H2A.Z biology by identifying its manifold binding proteins and
their functional roles in gene regulation\, cell cycle progression and org
anismal development.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/5/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Detlef Weigel (Max Planck Institute for Developmental Bi
ology)
DTSTART:20201125T090000Z
DTEND:20201125T110000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/6
DESCRIPTION:Title: Epistasis\, the Spice of Life (and Evolution) - Lessons from the study of
the plant immune system\nby Prof. Dr. Detlef Weigel (Max Planck Insti
tute for Developmental Biology) as part of Colloquium zooming Molecular &
Cellular Biology LUMS\n\n\nAbstract\nMy group is addressing fundamental qu
estions in evolutionary biology\, using both genome- and phenotype-first a
pproaches. A few years ago\, we discovered that Arabidopsis thaliana is a
great model for the study of hybrid necrosis. This widespread syndrome of
hybrid failure in plants is caused by plant paranoia – regardless of the
presence of enemies\, plants “think” they are being attacked by patho
gens. Over the past decade\, we have studied in detail the underlying gene
tics\, finding that often one or two loci encoding NLR immune receptors ar
e causal. NLRs make up the most variable gene family in plants\, and it is
not surprising that they are often involved in genome-genome conflicts. H
ybrid necrosis results when NLR genes meet that have not been co-adapted.
This has in turn raised the question of the scale of NLR diversity\, and o
ur goal for the next decade is to understand the genomic and geographic pa
tterns of immune system and especially NLR diversity. In 2018\, we initiat
ed a project\, PATHO(gens in Arabi)DOPSIS\, in which we aim to describe ge
netic diversity in the host A. thaliana and two of its important pathogens
\, the generalist Pseudomonas sp. and the specialist Hyaloperonospora arab
idopsidis. The long-term vision is to produce maps of resistance alleles i
n the host\, and of effector alleles in the pathogens\, in order to learn
when the pathogens win in a wild plant pathosystem – and when the hosts
prevail.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/6/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Juan Dominguez Bendala (University of Miami)
DTSTART:20201113T150000Z
DTEND:20201113T160000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/7
DESCRIPTION:Title: Advances in pancreatic beta-cell regeneration\nby Prof. Dr. Juan Domi
nguez Bendala (University of Miami) as part of Colloquium zooming Molecula
r & Cellular Biology LUMS\n\n\nAbstract\nLoss of β-cell mass and insulin-
producing ability is a major challenge in type 1 diabetic patients\, and
β-cells have notoriously low proliferating rates in adult humans. Therape
utic approaches that could lead to even partial restoration of the insulin
-producing ability of the pancreas would address a major therapeutic need.
The concept that the exocrine compartment of the pancreas harbors progen
itor cells with the ability to give rise to new β-cells through different
iation has been debated for years. Our work has focused on the description
and characterization of a novel population of multipotent BMP-7-responsiv
e progenitor-like cells within the human exocrine pancreas with the potent
ial to generate functional endocrine cells. These cells are characterized
by the expression of PDX1 and ALK3\, a canonical BMP receptor. We also con
firmed that these cells are present in the mouse pancreas\, which affords
us the possibility of studying endogenous regeneration in a setting not in
volving transplantation. Importantly\, preliminary analysis of samples fro
m the nPOD tissue network supports the concept that these cells are presen
t in patients who have had T1D for many years\, thus opening the possibili
ty of developing regenerative therapies for T1D. In this talk\, we will pr
esent our general strategies to: (a) Expand the high-resolution characteri
zation of the human pancreatic progenitor cell niche by single-cell analyt
ical techniques (Qadir et al\, PNAS\, 2020)\; and (b) Explore real-time β
-cell regeneration in human pancreatic slices (Qadir et al.\, Nature Commu
nications\, 2020). We will also briefly discuss our parallel studies on th
e CRISPR/cas9-mediated insertion of “kill switches” into human pluripo
tent stem cells to enhance their safety and efficacy in the context of ong
oing and future clinical trials. Taken together\, the topics discussed in
today’s seminar will present a clear roadmap towards the implementation
of state-of-the-art regenerative medicine approaches in the clinical arena
.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/7/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Jernej Ule (Francis Crick Institute)
DTSTART:20210108T100000Z
DTEND:20210108T110000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/8
DESCRIPTION:Title: RNA Biology at the crossroads of evolution and disease\nby Prof. Dr.
Jernej Ule (Francis Crick Institute) as part of Colloquium zooming Molecul
ar & Cellular Biology LUMS\n\n\nAbstract\nThe talk will introduce the tech
niques that can be used to investigate the assembly and function of ribonu
cleoprotein complexes (RNPs). This includes iCLIP\, a method combining mul
ti-step biochemistry and computational biology to obtain a comprehensive m
ap of protein-RNA interactions within cells. I will also present our study
of disease-causing mutations in TDP-43\, a protein that is often mutated
in amyotrophic lateral sclerosis. The mutations tend to be located within
intrinsically disordered regions\, and I will present the roles of these r
egions in fine-tuning the RNA binding properties and functions of the prot
ein. Moreover\, I will present our work on the roles that transposable ele
ments play in RNP assembly. I will discuss how these aspects of protein-RN
A interactions contribute to regulatory variation\, and thus play importan
t roles in evolution and disease.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/8/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Helge Grosshans (Friedrich Miescher Institute for Biomed
ical Research)
DTSTART:20210111T090000Z
DTEND:20210111T100000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/9
DESCRIPTION:Title: Properties and Functioning of a Developmental Clock\nby Prof. Dr. Hel
ge Grosshans (Friedrich Miescher Institute for Biomedical Research) as par
t of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nT
he development of an animal requires proper temporal synchronization of di
verse events\, facilitated by developmental clocks. How such clocks functi
on is only beginning to emerge. What are their properties? What are the co
mponents that make them run\, and how are they wired? To solve these quest
ions\, we investigate developmental timing in the roundworm C. elegans\, w
here we can exploit our recent discovery that thousands of genes oscillate
in expression during larval development. Such extensive and robust molecu
lar clock output\, combined with powerful tools for genetic manipulation a
nd screening\, makes C. elegans uniquely suited for dissecting the underly
ing clock mechanism. I will report how our work combining genomics\, genet
ic and high-throughput single animal-based approaches with theory has unco
vered a developmental clock with unusual checkpoint properties.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/9/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Giacomo Cavalli (Institute of Human Genetics)
DTSTART:20210115T090000Z
DTEND:20210115T100000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/10
DESCRIPTION:Title: Principles and functional role of 3D genome folding\nby Prof. Dr. Gi
acomo Cavalli (Institute of Human Genetics) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe eukaryotic genome fol
ds in 3D in a hierarchy of structures\, including nucleosomes\, chromatin
fibers\, loops\, chromosomal domains (also called TADs)\, compartments and
chromosome territories that are highly organized in order to allow for st
able memory as well as for regulatory plasticity\, depending on intrinsic
and environmental cues. Our lab has provided evidence suggesting that the
formation of TADs and chromatin loops can assist gene regulation\, both in
Drosophila and in mouse cells. Furthermore\, cellular stress\, such as re
plicative or oncogene-induced senescence\, can induce a massive nuclear re
organization that can affect gene expression. However\, the physical natur
e of compartments\, TADs and loops remain elusive and single-cell studies
are critically required to understand it. We characterized chromatin foldi
ng in single cells using super-resolution microscopy\, revealing structura
l features inaccessible to cell-population analysis. TADs range from conde
nsed and globular objects to stretched conformations. The physical insulat
ion associated with their borders is variable between individual cells\, y
et chromatin intermingling is enriched within TADs compared to adjacent TA
Ds in a large majority of cells. The spatial segregation of TADs is furthe
r exacerbated during cell differentiation. Favored interactions within TAD
s are regulated by cohesin and CTCF through distinct mechanisms. Furthermo
re\, super-resolution imaging revealed that TADs are subdivided into discr
ete nanodomains. Altogether\, these results provide a physical basis for t
he folding of individual chromosomes at the nanoscale. Our progress in the
se fields will be discussed.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/10/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Tony Hunter (Salk Institute for Biological Studies)
DTSTART:20210120T040000Z
DTEND:20210120T050000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/11
DESCRIPTION:Title: New Signal Transduction Targets for Cancer Therapy\nby Prof. Dr. Ton
y Hunter (Salk Institute for Biological Studies) as part of Colloquium zoo
ming Molecular & Cellular Biology LUMS\n\n\nAbstract\nPancreatic ductal ad
enocarcinoma (PDAC) has a dismal prognosis with few treatment options. We
have identified leukemia inhibitory factor (LIF)\, a stem cell factor\, as
a key paracrine factor\, secreted mainly by activated cancer-associated-f
ibroblasts (CAFs) in the tumor micro-environment (TME)\, that acts on panc
reatic tumor cells to maintain a stem cell-like population. Blockade of LI
F with a neutralizing monoclonal antibody (mAb) slows tumor progression in
the KPC mouse model of PDAC and augments efficacy of gemcitabine chemothe
rapy treatment to prolong survival. LIF levels are strongly elevated in bo
th mouse and human pancreatic tumor tissue\, and LIF is also is detected i
n serum from tumor-bearing mice and human PDAC patients\, suggesting its u
se as both as a biomarker and as a therapeutic target. In addition its act
ion on tumor cells\, we have found that LIF acts on myeloid cells in the i
mmune microenvironment to sustain a protumorigenic population of tumor-ass
ociated macrophages.\n\n \n\nHistidine phosphorylation\, the so-called “
hidden phosphoproteome”\, is poorly characterized. To study histidine ph
osphorylation we generated mAbs that selectively recognize the 1-pHis and
3-pHis-isoforms\, and have determined the structural basis of antibody rec
ognition of pHis. We have used these mAbs for immunoblotting and immunoflu
orescence staining to detect increased levels of pHis proteins in human ce
ll lines\, and also to survey the pHis proteome and identify new sites of
histidine phosphorylation. Using these mAbs\, we collaborated with Michael
Hall (Biozentrum\, Basel) to show that pHis levels are elevated in liver
tumors in a mouse model\, and in human hepatocellular carcinoma (HCC) tumo
r tissue\, as a result of reduced levels of the LHPP pHis phosphatase in t
umor tissue. On this basis\, we propose that LHPP serves as a tumor suppre
ssor in HCC\, and that histidine phosphorylation can act as a cancer drive
r. Consistently\, we have recently observed elevated levels of pHis protei
ns in PDAC stromal cells.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/11/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Mitzi Kuroda (Harvard University)
DTSTART:20210201T130000Z
DTEND:20210201T140000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/12
DESCRIPTION:Title: Bivalent Polycomb Complexes as Master Switches of Developmental Gene Reg
ulation\nby Prof. Dr. Mitzi Kuroda (Harvard University) as part of Col
loquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe genom
es of higher organisms are annotated by chromosomal proteins and histone m
odifications\, which delineate active genes\, regulatory elements\, and si
lent regions. This annotation is critical for proper cell type specificati
on\, and an ongoing challenge is to decipher the rules that establish and
maintain chromatin organization. Our studies of the highly conserved Polyc
omb group (PcG) epigenetic regulators in Drosophila has led my lab to prop
ose a model in which the Polycomb Repressive Complex 1 (PRC1) and classica
l co-activators form ‘bivalent’ protein complexes on transcriptionally
poised developmental genes. We speculate that these function as ‘master
switches’ that are responsive to the amount of local acetylation or dea
cetylation activities recruited by cell type specific DNA binding factors\
, leading to stable but reversible activation or repression\, respectively
. Our model is based on chromatin crosslinking\, affinity purification\, a
nd mass spectrometry experiments\, in which Drosophila PRC1 strongly inter
acts with classical co-activators\, dBRD4 and dMOZ. We are currently explo
ring potential parallels in mammalian development\n\nOrganizers can be con
tacted at m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/12/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Gregory Gibson (Georgia Institute of Technology)
DTSTART:20210209T130000Z
DTEND:20210209T140000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/13
DESCRIPTION:Title: Transcriptomics for Personalized Medicine\nby Prof. Dr. Gregory Gibs
on (Georgia Institute of Technology) as part of Colloquium zooming Molecul
ar & Cellular Biology LUMS\n\n\nAbstract\nTranscriptomics is the study of
gene expression. It has enormous potential to understand the molecular ba
sis of disease and to help guide therapeutic intervention. These day\, RN
A sequencing (scRNAseq) can be used to profile gene expression in thousand
s of individual cells\, allowing reserarchers to characterize which cell t
ypes are modified in patients destined to progress to complicated disease.
By combining transcriptomics with genome-wide association studies (TWAS)
\, we can identify causal genes that are involved in pathogenesis. I will
discuss recent findings from my group in relation to inflammatory bowel d
isease\, a chronic disease of the gut which is increasing in prevalence al
l over the world. Specific genetic signatures predict disease progression
\, including the need for colectomy\, and might be used to guide medicatio
n usage to those in most need or most likely to respond. I will also desc
ribe a new approach to studying how polygenic risk interacts with environm
ental exposures to influence risk of complicated disease.\n\nOrganizers ca
n be contacted at m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoom
link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/13/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Susan Wessler (University of California Riverside)
DTSTART:20210224T040000Z
DTEND:20210224T050000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/14
DESCRIPTION:Title: Understanding the strategies evolved by a very successful transposable e
lement\nby Prof. Dr. Susan Wessler (University of California Riverside
) as part of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbs
tract\nTransposable elements (TEs) achieve high copy numbers through waves
of amplification called bursts.\nFor a TE to successfully burst it must b
e able to significantly increase its copy number without killing its\nhost
or being silenced by genome surveillance (epigenetic) mechanisms. However
\, because the vast majority of TE\nbursts have been inferred after the fa
ct – via computational analysis of whole genome sequence – the\nstealt
h features they require for success have remained largely undiscovered. So
me features have recently\nbeen discovered by analyzing active bursts of t
he miniature inverted repeat transposable element (MITE)\nmPing and its au
tonomous partner Ping in four strains of domesticated rice (Oryza sativa\,
temperate\njaponica). First\, mPing targets genic regions but avoids exon
sequences\, thus minimizing harm to the\nhost. Second\, because mPing doe
s not share coding sequences with Ping\, increases in its copy number and\
nhost recognition of its sequences do not silence Ping genes\, thus allowi
ng the continuous production of\nthe proteins necessary to sustain the bur
st for decades.\n\nAdditional insights into the mPing burst comes from ana
lyses of an extensive collection of rice genomes\nincluding 3000 domestica
ted strains and a recombinant inbred population. While the survey of 3000\
nstrains revealed that the burst is very recent and is restricted to a few
closely related accessions\, analysis\nof the sequences of 272 recombinan
t inbred lines demonstrated the potential of mPing to rapidly spread\nunim
peded through a large population and increase the frequency of structural
variations.\n\nOrganizers can be contacted at m.tariq@lums.edu.pk or 22100
032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/14/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Steve Henikoff (Fred Hutchinson Cancer Research Center)
DTSTART:20210303T040000Z
DTEND:20210303T050000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/15
DESCRIPTION:Title: Genome-wide mapping of protein-DNA interaction dynamics\nby Prof. Dr
. Steve Henikoff (Fred Hutchinson Cancer Research Center) as part of Collo
quium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nWe recently
introduced new tools for high-resolution genome-wide chromatin profiling
and have applied them to study chromatin organization and dynamics in a va
riety of model systems\, including yeast\, flies and mammals. Among the qu
estions addressed are: How do transcription factors find their binding sit
es in DNA packaged into nucleosomes? How are nucleosomes depleted from gen
e regulatory regions? What is the relationship between nucleosome depositi
on pathways and chromatin deregulation in disease? Our findings illustrate
ways in which chromatin dynamics can play a central role in regulating ge
ne expression and silencing.\n\nOrganizers can be contacted at m.tariq@lum
s.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/15/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Hiten Madhani (University of California San Francisco)
DTSTART:20210305T050000Z
DTEND:20210305T060000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/16
DESCRIPTION:Title: Epigenetic memory over geological timescales\nby Prof. Dr. Hiten Mad
hani (University of California San Francisco) as part of Colloquium zoomin
g Molecular & Cellular Biology LUMS\n\n\nAbstract\nI will describe our rec
ent work examining the maintenance of DNA methylation in the yeast Cryptoc
occus neoformans. In many species\, DNA methylation is established by a d
e novo enzyme that can methylate unmethylated DNA. Such enzymes act in na
rrow developmental windows and this initial activity is subsequently propa
gated epigenetically via a maintenance enzyme specific for hemimethylated
DNA. I will describe a species which lacks a de novo enzyme and only harb
ors a maintenance enzyme.\n\nOrganizers can be contacted at m.tariq@lums.e
du.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/16/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Denis Duboule (University of Geneva)
DTSTART:20210322T090000Z
DTEND:20210322T100000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/17
DESCRIPTION:Title: Hox gene regulation in embryos and pseudo-embryos\nby Prof. Dr. Deni
s Duboule (University of Geneva) as part of Colloquium zooming Molecular &
Cellular Biology LUMS\n\n\nAbstract\nDuring vertebrate development\, clus
tered Hox genes are activated in a precise time-sequence\, leading to patt
erns necessary to properly establish the body plan. The mechanism underlyi
ng this in cis timing phenomenon has remained unknown ever since its obser
vation in 1989\, due to the difficulty to approach it using early gastrula
ting mouse embryos. I will discuss an alternative possibility\, which is t
o use pseudo-embryos produced out of ES cells (referred to as gastruloids)
to address this now 30 years old question and will show some preliminary
data indicating that this system may allow us to more efficiently tackle t
his issue in the next few years to come.\n\nOrganizers can be contacted at
m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/17/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Wendi Bickmore (University of Edinburgh)
DTSTART:20210407T100000Z
DTEND:20210407T110000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/18
DESCRIPTION:Title: The role of spatial proximity in genome regulation\nby Prof. Dr. Wen
di Bickmore (University of Edinburgh) as part of Colloquium zooming Molecu
lar & Cellular Biology LUMS\n\n\nAbstract\nImaging and genomic technologie
s have opened up large-scale interrogation of 3D genome organisation in th
e cell nucleus. This has revealed multiple layers of organisation and at d
ifferent scales\, including distal interactions of genome compartments\, t
opologically associating domains (TADs) and specific cis interactions betw
een either active or repressive elements. Progress is being made toward un
derstanding the molecular mechanisms that mediate these layers of organisa
tion. However\, understanding the functional significance of 3D organisati
on across genomic scales lags behind. To what extent does 3D organisation
drive genome regulation\, or are some aspects of 3D organisation simply an
emergent property of genome and protein functions? In this talk I will de
scribe our efforts to determine the functional significance of the 3D geno
me – from the action of polycomb complexes in bridging distal interactio
ns between repressed loci\, to the role of TADs and enhancer-promoter prox
imity in enhancer-driven gene activation.\n\nOrganizers can be contacted a
t m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/18/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Dirk Schubeler (Friedrich Miescher Institute for Biomedi
cal Research)
DTSTART:20210421T080000Z
DTEND:20210421T090000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/19
DESCRIPTION:Title: Finding your place: Transcription factors as sensors and modifiers of ch
romatin\nby Prof. Dr. Dirk Schubeler (Friedrich Miescher Institute for
Biomedical Research) as part of Colloquium zooming Molecular & Cellular B
iology LUMS\n\n\nAbstract\nTranscription factors only bind a minority of t
heir motifs in large mammalian genomes. One potential explanation is that
many motifs are not accessible for binding due to the action of chromatin
and DNA methylation. We are using mammalian stem cell models to understand
this important interplay between gene regulation\, chromatin structure an
d DNA methylation. We study the dynamics of the epigenome and test regulat
ory models in cellular models by genetic perturbation and genome editing a
pproaches. I will discuss our recent efforts in understanding how the sens
itivity to DNA methylation can limit transcription factor binding in the c
ontext of the cell\, the identification of a novel\, strong activating fac
tor and how transcripton factors rely on specific chromatin remodelers for
access to their binding sites.\n\nOrganizers can be contacted at m.tariq@
lums.edu.pk or 22100032@lums.edu.pk for the zoom link\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/19/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Robert Weinberg (Massachusetts Institute of Technology)
DTSTART:20210311T140000Z
DTEND:20210311T150000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/20
DESCRIPTION:Title: Mechanisms of the Malignant Progression of Carcinomas\nby Prof. Dr.
Robert Weinberg (Massachusetts Institute of Technology) as part of Colloqu
ium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe formation
of primary tumors depends in no small part on the acquisition by evolving
primary tumor cells of a series of somatically mutated alleles. However\
, the last step of tumor progression involves the processes of invasion an
d metastasis and it has been less clear precisely how these traits are acq
uired. As will be described\, these phenotypes of high-grade malignancy ar
e consequences of the actions of non-genetic\, i.e\,\, epigenetic changes
in cancer cells that are mediated by induction of the cell-biological prog
ram termed the epithelial-mesenchymal transition\, which confers many of t
he traits that are associated traditionally with the changes associated wi
th the carcinoma cells of high-grade tumors. In addition\, induction of th
is program is associated with the acquisition of stemness\, that is\, tumo
r-initiating potential\, which is essential for successful metastasis form
ation. These various non-genetic processes will be discussed!\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/20/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Shiv Grewal (National Institutes of Health)
DTSTART:20210526T120000Z
DTEND:20210526T130000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/21
DESCRIPTION:Title: Epigenetic genome control by RNA-based mechanisms\nby Prof. Dr. Shiv
Grewal (National Institutes of Health) as part of Colloquium zooming Mole
cular & Cellular Biology LUMS\n\n\nAbstract\nGenome-wide sequencing of the
human genome and several model organisms has greatly facilitated research
into genome structure and function. Much attention is now focused on und
erstanding how the functional organization of the genome supports translat
ion of genetic information into formation of different cell types during d
evelopment\, and how it contributes to disease progression. We have shown
previously that distinct histone methylation patterns organize chromosome
s into “open” euchromatin (H3K4me) and “closed” heterochromatin (H
3K9me) domains\, to modulate use of the genome. Our work has also reveale
d that heterochromatin can be targeted by RNAi machinery and/or by pathway
s requiring RNA elimination and transcription termination factors. Moreov
er\, we find that RNA processing factors and heterochromatin machinery are
part of an adaptive cellular mechanisms that can reprogram the genome in
response to changes in environmental growth conditions and developmental s
ignals. Our most recent work on the assembly and epigenetic inheritance o
f silenced chromatin domains\, essential for proper gene regulation during
development will be presented.\n\nThe organizers can be contacted at 2210
0032@lums.edu.pk for the zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/21/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Ellen Rothenberg (California Institute of Technology)
DTSTART:20210624T040000Z
DTEND:20210624T060000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/22
DESCRIPTION:Title: Gene network and epigenetic mechanisms controlling the generation of T l
ymphocytes\nby Prof. Dr. Ellen Rothenberg (California Institute of Tec
hnology) as part of Colloquium zooming Molecular & Cellular Biology LUMS\n
\n\nAbstract\nT lymphocytes are vital components of the immune system in h
umans and other mammals. They are generated by multiple waves of blood ce
ll precursors that migrate from the bone marrow to a special organ\, the t
hymus\, where the stem cell-like precursor cells encounter signals that ca
use them to differentiate into T cells. This process is important for heal
th by providing resistance to infection and cancer\, and it is also very i
lluminating as a model system to show how environmental signaling\, endoge
nously expressed transcription factors\, and epigenetic chromatin changes
can work together in an orderly\, stepwise process to convert cells effici
ently from stem-like cells to effective\, useful differentiated cells. We
can “zoom in” to observe and dissect this process through powerful in
vitro culture systems that mimic the thymus in an open format\, which all
ows the developing cells to be observed and manipulated. \nThe Rothenberg
lab has focused on answering three kinds of questions. First\, how do the
transcription factors in these cells act in a cascade\, so that each tran
scription factor works to activate or shut off other transcription factors
in an orderly way\, which then themselves change the expression of anothe
r set of genes? Second\, how does the epigenetic state of the chromatin a
ffect what these transcription factors can do at a given stage\, and how d
o the factors themselves alter the epigenetic state to allow differentiati
on to proceed? Third\, how do these mechanisms explain the high efficiency
but slow speed of this developmental process? The talk will show how rec
ent results shed light on these questions.\n\nOrganizers can be contacted
at 22100032@lums.edu.pk for the Zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/22/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Mariana Wolfner (Cornell University)
DTSTART:20211005T130000Z
DTEND:20211005T143000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/23
DESCRIPTION:Title: Activating eggs and stimulating reproduction: the molecular view from Dr
osophila (and beyond).\nby Prof. Dr. Mariana Wolfner (Cornell Universi
ty) as part of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nA
bstract\nSuccessful reproduction in internal-fertilizing animals requires
molecular modification of both the oocyte and the female. Oocytes must “
activate”\, transitioning from meiotic and molecular arrest to the totip
otency of early embryogenesis after fertilization. The female’s physiolo
gy must change to support her reproductive success\, egg production\, and
her progeny. Versions of these phenomena are universal\, including in huma
n fertility and that of insect vectors of diseases like Dengue and Zika. B
ut they can be particularly well dissected using model-organisms such as D
rosophila fruit flies. This talk will present results from studies using t
his model to dissect mechanisms that activate eggs\, and others to elucida
te mechanisms that stimulate the female’s reproductive capacity. We will
see that egg activation is accompanied by a rise in calcium levels in the
egg which\, in turn\, modifies the egg’s proteins to transition to embr
yogenesis. We will then consider how the female’s physiological state is
modified by seminal proteins that she receives during mating\, and how th
ese male-derived proteins act to stimulate her egg production\, including
a signal that activates her eggs. The talk will conclude by summarizing ho
w these findings inform our understanding of mechanisms of egg activation
and seminal protein actions in animals more generally.\n\nOrganizers can b
e reached out at 22100032@lums.edu.pk for the Zoom link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/23/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. David Baulcombe (Cambridge University)
DTSTART:20211013T090000Z
DTEND:20211013T103000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/24
DESCRIPTION:Title: RNA silencing\, disease resistance and non-Mendelian inheritance\nby
Prof. Dr. David Baulcombe (Cambridge University) as part of Colloquium zo
oming Molecular & Cellular Biology LUMS\n\n\nAbstract\nRNA silencing was d
iscovered by accident as a virus defense mechanism but our current underst
anding is that it is a family of related mechanisms affecting transposons
and gene expression. In this talk I will describe how\, in defense\, RNA s
ilencing is relevant as more than protection against viruses – it influe
nces resistance against cellular as well as viral pathogens and it operate
s as part of a network of mechanisms in which the different layers of the
plants innate immune system are connected and integrated. I will also desc
ribe how RNA silencing can influence non-Mendelian inheritance patterns of
gene expression in the progeny of crosses between genetically distinct pa
rents.\n\nOrganizers can be contacted at 22100032@lums.edu.pk for the Zoom
link.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/24/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Gregory Hannon (Cambridge University)
DTSTART:20211119T110000Z
DTEND:20211119T123000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/25
DESCRIPTION:Title: A small RNA-based innate immune system guards the integrity of germ cell
genomes\nby Prof. Dr. Gregory Hannon (Cambridge University) as part o
f Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nPIWI
-family proteins and their associated small RNAs (piRNAs) act in an evolut
ionarily conserved innate immune mechanism that provides an essential prot
ection for germ cell genomes against the activity of mobile genetic elemen
ts. piRNA populations comprise a molecular definition of transposons that
permits them to be distinguished from host genes and selectively silenced.
piRNAs can be generated in two distinct ways. Primary piRNAs emanate from
discrete genomic loci\, termed piRNA clusters\, and appear to be derived
from long\, single-stranded precursors. The biogenesis of primary piRNAs i
nvolves at least two nucleolytic steps. Zucchini cleaves piRNA cluster tra
nscripts to generate monophosphorylated piRNA 5’ ends. piRNA 3’ ends a
re likely formed by exonucleolytic trimming\, after a piRNA precursor is l
oaded into its PIWI partner. Secondary piRNAs arise during the adaptive pi
ng-pong cycle\, with their 5’ termini being formed by the activity of PI
WIs themselves. At least in Drosophila\, piRNAs are maternally deposited a
nd transmit an epigenetic signal essential for the effective control of at
least some transposable elements. Our continuing efforts combine genetics
\, biochemistry\, structural biology\, and evolutionary and computational
approaches to understand how the piRNA pathway effectively discriminates s
elf from non-self at the genomic level.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/25/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Norbert Perrimon (Harvard University)
DTSTART:20220325T140000Z
DTEND:20220325T150000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/26
DESCRIPTION:Title: Inter-organ communication: Studies in Drosophila\nby Prof. Dr. Norbe
rt Perrimon (Harvard University) as part of Colloquium zooming Molecular &
Cellular Biology LUMS\n\n\nAbstract\nI will discuss our ongoing studies t
o identify and characterize communication pathways between major organs in
Drosophila. Organ-to-organ communications are critical to living systems
and play major roles in homeostasis. For example\, the vertebrate CNS rece
ives information regarding the status of peripheral metabolic processes vi
a hormonal signaling and direct macromolecular sensing. In addition\, skel
etal muscles produce various myokines that influence metabolic homeostasis
\, lifespan\, and the progression of age-related diseases and aging in non
-muscle tissues. Using genetic screening\, transcriptome analyses and pro
teomic approaches\, we are identifying and characterizing secreted factors
by which organs communicate their physiological state to others in both h
omeostasis and altered metabolism\, as well as tumor models. These studies
are providing fundamental insights into how biological processes observed
in one tissue/organ (e.g.\, decreased cellular metabolism\, mitochondrial
dysfunction) influence the state of other tissues/organs.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/26/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Cedric Maurange (Institute of Developmental Biology of M
arseilles)
DTSTART:20220608T090000Z
DTEND:20220608T103000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/27
DESCRIPTION:Title: Deconstructing the principles of cellular hierarchy in tumors with a dev
elopmental origin\nby Prof. Dr. Cedric Maurange (Institute of Developm
ental Biology of Marseilles) as part of Colloquium zooming Molecular & Cel
lular Biology LUMS\n\n\nAbstract\nPediatric cancers are different from adu
lt cancers in that they carry much fewer genetic lesions but are able to p
rogress extremely rapidly. In addition\, brain cancers are over-represente
d in children. Recent data has demonstrated that pediatric brain cancers o
ften originate during embryonic and fatal stages\, and aberrantly recapitu
late sub-parts of developmental programs. It has been proposed that such t
umors are « locked » into perpetual development. Yet it is often unclear
why these developmental programs become mis-regulated during the course o
f development and how they are coopted to promote tumorigenesis. We are ad
dressing these questions using a Drosophila model of neural tumors with a
developmental origin\, resembling in many aspect pediatric cancers in huma
n. Our work has identified the coopted developmental program that sustains
tumor growth and has deciphered their hierarchical cellular organization.
During my talk\, I will present our recent finding that epigenetic regula
tors of the PRC2 and MLL1/2-COMPASS complexes regulate this hierarchy\, an
d how their inactivation can trigger plasticity and cancer stem cell heter
ogeneity.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/27/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Danny Reinberg (New York University)
DTSTART:20220621T130000Z
DTEND:20220621T140000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/28
DESCRIPTION:Title: Polycomb\, Inheritance and Disease\nby Prof. Dr. Danny Reinberg (New
York University) as part of Colloquium zooming Molecular & Cellular Biolo
gy LUMS\n\n\nAbstract\nEpigenetics encompasses changes in gene expression
profiles that occur without alterations in the genomic DNA sequence of a c
ell. This arises from the dynamic processes that structure regions of chro
mosomal DNA through a range of compaction in eukaryotes. The altered patte
rn of gene expression is pivotal to cellular differentiation and developme
nt and is inherited by daughter cells thereby maintaining the integrity\,
specifications\, and functions for a given cell type. Aberrancies in this
epigenetic process give rise to perturbations that are also inherited and
disruptive to normal cellular properties.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/28/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Monica P. Colaiacovo (Harvard Medical School)
DTSTART:20221109T140000Z
DTEND:20221109T150000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/29
DESCRIPTION:Title: Location and numbers: how recombination and our chemical landscape conve
rge on meiosis\nby Prof. Dr. Monica P. Colaiacovo (Harvard Medical Sch
ool) as part of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\n
Abstract\nResearch in our laboratory is focused on understanding the regul
ation of mechanisms that promote accurate chromosome segregation during me
iosis\, such as recombination\, and how exposure to endocrine-disrupting c
hemicals (EDCs) affect these mechanisms. Errors in achieving accurate chro
mosome segregation during meiosis can result in the formation of aneuploid
gametes (i.e.\, eggs and sperm carrying an incorrect number of chromosome
s)\, which is associated with miscarriages\, stillbirths\, infertility\, a
nd birth defects. Our team has directly demonstrated in a metazoan (the ne
matode C. elegans) how the position of DNA double-strand breaks and crosso
ver recombination events are critical for accurate chromosome segregation
and how exposure to an abundantly used plasticizer (DEHP) alters this regu
lation. Ongoing studies are examining what factors regulate the distributi
on of recombination events and how other EDCs differentially affect female
and male meiosis\, leading to embryonic lethality and infertility.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/29/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Dietrich M. Egli (Columbia University)
DTSTART:20221110T080000Z
DTEND:20221110T090000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/30
DESCRIPTION:Title: Genome stability in embryonic development and reprogramming\nby Prof
. Dr. Dietrich M. Egli (Columbia University) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe events occurring in
the beginning of human development are highly consequential for everything
that follows\, but remain poorly understood and little investigated. Most
human embryos fail to develop shortly after fertilization. This inefficie
ncy in development is primarily caused by an unstable genome\, resulting i
n aneuploidies\, DNA damage\, cell cycle arrest\, and in developing embryo
s likely novel mutations. I will present our novel insight on how the embr
yo replicates its DNA and how inefficiencies in DNA repair in the embryo s
hape fertility as well as our health throughout life.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/30/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Fred Winston (Harvard Medical School)
DTSTART:20230203T130000Z
DTEND:20230203T140000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/31
DESCRIPTION:Title: Analysis of factors that control transcriptional fidelity and chromatin
structure\nby Prof. Dr. Fred Winston (Harvard Medical School) as part
of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nNuc
leosomes are barriers for transcription. To help to alleviate these barrie
rs\, a class of factors called histone chaperones modulates histone-DNA in
teractions. Our work has focused on set of three histone chaperones that a
re essential for viability and that are conserved from yeast to humans. Ou
r studies\, using S. cerevisiae as a model system\, have shown that these
three factors\, Spt6\, Spn1\, and FACT\, are broadly required for the fide
lity of transcription and the integrity of chromatin structure. While all
three histone chaperones are vital for growth\, we have found unexpected c
onnections between their functions that suggest that they interact in a ne
twork that is critical for their functions in transcription\, as well as o
ther chromatin-templated functions including DNA replication and genome st
ability.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/31/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Sue Biggins (Fred Huch Cancer Center)
DTSTART:20230306T150000Z
DTEND:20230306T160000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/32
DESCRIPTION:Title: How do cells inherit the right chromosomes?\nby Prof. Dr. Sue Biggin
s (Fred Huch Cancer Center) as part of Colloquium zooming Molecular & Cell
ular Biology LUMS\n\n\nAbstract\nThe precise regulation of cell division i
s critical to processes such as self-renewal\, proliferation and developme
nt. A key event in the cell cycle is the partitioning of every pair of dup
licated chromosomes to daughter cells. Chromosomes segregate using their k
inetochores\, the specialized protein structures that are assembled on cen
tromeric DNA sequences and attach to spindle microtubules. I will discuss
our recent advances in isolating and reconstituting kinetochores and stud
ying their behavior by biochemical and biophysical techniques in vitro. Th
is work showed that tension directly regulates the activity of the Aurora
B kinase. In addition\, I will discuss our recent development of a single
molecule assay to monitor kinetochore assembly in real time and what it h
as revealed about the centromeric nucleosome and the specificity of the ce
ntromeric DNA\, work that ultimately is critical to understanding how cell
s maintain genomic stability.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/32/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Constance Cepko (Harvard Stem Cell Institute)
DTSTART:20230329T103000Z
DTEND:20230329T113000Z
DTSTAMP:20260422T225827Z
UID:MCB_LUMS/33
DESCRIPTION:Title: Gene Therapy to Prolong Vision\nby Prof. Dr. Constance Cepko (Harvar
d Stem Cell Institute) as part of Colloquium zooming Molecular & Cellular
Biology LUMS\n\n\nAbstract\nThere are >200 human disease genes leading to
blindness. Although gene therapy in which each disease gene is augmented o
r edited is possible\, this approach would be extremely expensive and logi
stically challenging. To provide an alternative\, more general approach\,
our laboratory has been analyzing mouse models of blindness\, looking for
problems that are common across genotypes. We were particularly interested
in mouse models for retinitis pigmentosa (RP)\, as it is well modeled in
mice\, relative to humans. In RP\, the disease starts with the expression
of mutant genes in rod photoreceptors\, the cell type that initiates dim l
ight vision\, leading to poor night vision. However\, color vision\, which
originates with cone photoreceptors\, is normal at birth. Over time\, con
es become affected due to bystander effects from rod loss. This causes col
or blindness and can lead to total blindness. Other cells also are affecte
d by the loss of rods: the retinal pigmented epithelial cells (RPE)\, whic
h provide various types of support to rods and cones. Studies of these mou
se models led to the hypothesis that the bystander effects include: oxidat
ive damage\, metabolic shortcomings\, and inflammation. To combat these pr
oblems\, many different types of genes were delivered using adeno-associat
ed viruses (AAV). Genes that fight inflammation\, a transcription factor t
hat regulates genes that fight oxidative damage\, and genes that provide m
etabolic support were found to prolong cone and RPE survival as well as vi
sion across 3 strains of RP mice.\n
LOCATION:https://researchseminars.org/talk/MCB_LUMS/33/
END:VEVENT
END:VCALENDAR