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BEGIN:VEVENT
SUMMARY:Prof. Dr. Oliver Bell (University of Southern California)
DTSTART:20200728T160000Z
DTEND:20200728T170000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/1
DESCRIPTION:Title: How cell fate decisions are maintained by Polycomb\nby Prof. D
r. Oliver Bell (University of Southern California) as part of Colloquium z
ooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nTranscriptional si
lencing by Polycomb group (PcG) proteins is a major paradigm for epigeneti
c inheritance from fly to human. The Polycomb Repressive Complexes PRC1 an
d PRC2 catalyse distinct chromatin modifications to enforce gene silencing
. However\, the mechanisms underlying the inheritence of transcriptional s
ilencing by different PRC complexes are not known. Addressing this questio
n has been extremely challenging due to technical limitations that do not
discern the initiation from sequence-independent maintenance of repression
. We have solved this problem by developing an approach to reversibly recr
uit PRC1 or PRC2 to transcriptionally inactive or active chromatin in mous
e embryonic stem cells. For the first time\, we directly and systematicall
y interrogate the ability of different PcG complexes to (1) form repressiv
e chromatin structure\, (2) initiate gene silencing\, and (3) maintain sil
encing. I will present an unexpected division of labour between different
PRC1 and PRC2 complexes in epigenetic silencing.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/2
DESCRIPTION:Title: How and where to assemble heterochromatin\, and why it is essentia
l for organismal survival\nby Prof. Dr. Susan Gasser (Freidrich Miesch
er Institute for Biomedical Research) as part of Colloquium zooming Molecu
lar & Cellular Biology LUMS\n\n\nAbstract\nThe establishment and maintenan
ce of chromatin domains shape the epigenetic memory of a cell\, with histo
ne H3 lysine 9 methylation (H3K(me) defining repressed heterochromatin. In
C. elegans\, SET-25 (SUV39/g9a) catalyzes to its targets. One requires re
cognition 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-in
dependent pathway makes up ~10% of SET-25 target sequences\, and most nota
bly includes intact transposons. Compared to single mutants\, met-2\;nrde-
3 double mutant enhances transposon transcription and embryonic lethality.
Whereas the targeting of SET-25 silences transposons\, whose expression c
ompromises development\, the targeting of MET-2/SET-DB1 is necessary to pr
event the promiscuous transcription of simple repeats. Simple repeat trans
cripts lead to R-loops and fork-associated damage\, that requires BRCA1 to
ensure survival. While the genome becomes unstable\, met-2 mutants show n
early normal developmental and differentiation patterns.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/2/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Dr. Stefan Schoenfelder (Babraham Institute\, Cambridge)
DTSTART:20200911T100000Z
DTEND:20200911T120000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/3
DESCRIPTION:Title: Functional Organization of the Genome in 3D\nby Dr. Stefan Sch
oenfelder (Babraham Institute\, Cambridge) as part of Colloquium zooming M
olecular & Cellular Biology LUMS\n\n\nAbstract\nThe three-dimensional orga
nisation of the genome is tightly linked to its function. The cell-type sp
ecific folding of the DNA enables gene regulatory elements\, including pro
moters and enhancers\, to interact\, in some cases bridging distances of h
undreds of kilobases. These enhancer-promoter contacts are thought to be c
rucial for gene expression control. I will discuss recent progress in the
methodology to map the 3D organisation of chromatin in mammalian nuclei ge
nome-wide\, illustrate on examples how enhancer-promoter contacts dynamica
lly respond to signalling cues and are rewired during cell fate transition
s\, and highlight some of the major challenges and open questions in the f
ield.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/3/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Peter Becker (LMU Munich)
DTSTART:20201009T070000Z
DTEND:20201009T090000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/4
DESCRIPTION:Title: Genetic & Epigenetic Mechanisms of X Chromosome Activation in Dros
ophila\nby Prof. Dr. Peter Becker (LMU Munich) as part of Colloquium z
ooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe process of X-c
hromosome dosage compensation in Drosophila involves boosting the transcri
ption of most genes on the X in male flies to match the transcription outp
ut of the two X chromosomes in females. Activation is achieved through his
tone acetylation of active gene chromatin by the histone acetyltransferase
MOF. MOF is recruited to its targets by the dosage compensation complex (
DCC). According to the prevalent model this involves genetic and epigeneti
c principles: the DCC first binds to a defined number of DNA sequence ele
ments\, the High Affinity Sites (HAS)\, which are exclusive to the X. The
activator then identifies and acetylates active gene chromatin in the nucl
ear neighborhood\, presumably through their epigenetic H3K36me3 signature.
\n\nDosage compensation happens gradually during early embryonic developme
nt and matures along with refined chromosome folding. Key to successful do
sage compensation is the property of the DCC to selectively bind the X chr
omosome. We continue to explore the molecular principles that allow such s
elective regulation. Most recently\, we made significant progress in ident
ifying and testing such principles by whole-genome chromatin reconstitutio
n in a cell-free system.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/4/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Sandra Hake (JLU Giessen)
DTSTART:20201016T070000Z
DTEND:20201016T090000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/5
DESCRIPTION:Title: Histones: How much variation do we need?\nby Prof. Dr. Sandra
Hake (JLU Giessen) as part of Colloquium zooming Molecular & Cellular Biol
ogy LUMS\n\n\nAbstract\nAll eukaryotes organize their DNA together with hi
stones and non-histone proteins into a highly complex nucleoprotein struct
ure called chromatin\, with the nucleosome as its monomeric subunit. Sever
al interconnected mechanisms have evolved to regulate DNA accessibility\,
including nucleosome replacement of canonical histones with specialized hi
stone variants. Deposition of histone variants can lead to profound chroma
tin structure alterations thereby influencing a multitude of biological pr
ocesses ranging from transcriptional regulation to genome stability. At th
e focus of our research is the evolutionary highly conserved histone varia
nt H2A.Z\, which has been extensively studied and shown to play a role in
gene expression\, DNA repair\, heterochromatin formation\, chromosome segr
egation and mitosis. But the mechanism(s) of how H2A.Z controls these dive
rse biological processes is not understood. Using state-of-the-art biochem
ical\, cell biological\, genome-wide and bioinformatics approaches we are
shedding light on H2A.Z biology by identifying its manifold binding protei
ns and their functional roles in gene regulation\, cell cycle progression
and organismal development.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/6
DESCRIPTION:Title: Epistasis\, the Spice of Life (and Evolution) - Lessons from the s
tudy of the plant immune system\nby Prof. Dr. Detlef Weigel (Max Planc
k Institute for Developmental Biology) as part of Colloquium zooming Molec
ular & Cellular Biology LUMS\n\n\nAbstract\nMy group is addressing fundame
ntal questions in evolutionary biology\, using both genome- and phenotype-
first approaches. A few years ago\, we discovered that Arabidopsis thalian
a is a great model for the study of hybrid necrosis. This widespread syndr
ome of hybrid failure in plants is caused by plant paranoia – regardless
of the presence of enemies\, plants “think” they are being attacked b
y pathogens. Over the past decade\, we have studied in detail the underlyi
ng genetics\, finding that often one or two loci encoding NLR immune recep
tors are causal. NLRs make up the most variable gene family in plants\, an
d it is not surprising that they are often involved in genome-genome confl
icts. Hybrid necrosis results when NLR genes meet that have not been co-ad
apted. This has in turn raised the question of the scale of NLR diversity\
, and our goal for the next decade is to understand the genomic and geogra
phic patterns of immune system and especially NLR diversity. In 2018\, we
initiated a project\, PATHO(gens in Arabi)DOPSIS\, in which we aim to desc
ribe genetic diversity in the host A. thaliana and two of its important pa
thogens\, the generalist Pseudomonas sp. and the specialist Hyaloperonospo
ra arabidopsidis. The long-term vision is to produce maps of resistance al
leles in 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://stable.researchseminars.org/talk/MCB_LUMS/6/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Juan Dominguez Bendala (University of Miami)
DTSTART:20201113T150000Z
DTEND:20201113T160000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/7
DESCRIPTION:Title: Advances in pancreatic beta-cell regeneration\nby Prof. Dr. Ju
an Dominguez Bendala (University of Miami) as part of Colloquium zooming M
olecular & Cellular Biology LUMS\n\n\nAbstract\nLoss of β-cell mass and i
nsulin-producing ability is a major challenge in type 1 diabetic patients\
, and β-cells have notoriously low proliferating rates in adult humans. T
herapeutic approaches that could lead to even partial restoration of the i
nsulin-producing ability of the pancreas would address a major therapeutic
need. The concept that the exocrine compartment of the pancreas harbors
progenitor cells with the ability to give rise to new β-cells through dif
ferentiation has been debated for years. Our work has focused on the descr
iption and characterization of a novel population of multipotent BMP-7-res
ponsive progenitor-like cells within the human exocrine pancreas with the
potential to generate functional endocrine cells. These cells are characte
rized by the expression of PDX1 and ALK3\, a canonical BMP receptor. We al
so confirmed that these cells are present in the mouse pancreas\, which af
fords us the possibility of studying endogenous regeneration in a setting
not involving transplantation. Importantly\, preliminary analysis of sampl
es from the nPOD tissue network supports the concept that these cells are
present in patients who have had T1D for many years\, thus opening the pos
sibility of developing regenerative therapies for T1D. In this talk\, we w
ill present our general strategies to: (a) Expand the high-resolution char
acterization of the human pancreatic progenitor cell niche by single-cell
analytical techniques (Qadir et al\, PNAS\, 2020)\; and (b) Explore real-t
ime β-cell regeneration in human pancreatic slices (Qadir et al.\, Nature
Communications\, 2020). We will also briefly discuss our parallel studies
on the CRISPR/cas9-mediated insertion of “kill switches” into human p
luripotent stem cells to enhance their safety and efficacy in the context
of ongoing and future clinical trials. Taken together\, the topics discuss
ed in today’s seminar will present a clear roadmap towards the implement
ation of state-of-the-art regenerative medicine approaches in the clinical
arena.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/7/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Jernej Ule (Francis Crick Institute)
DTSTART:20210108T100000Z
DTEND:20210108T110000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/8
DESCRIPTION:Title: RNA Biology at the crossroads of evolution and disease\nby Pro
f. Dr. Jernej Ule (Francis Crick Institute) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe talk will introduce t
he techniques that can be used to investigate the assembly and function of
ribonucleoprotein complexes (RNPs). This includes iCLIP\, a method combin
ing multi-step biochemistry and computational biology to obtain a comprehe
nsive map of protein-RNA interactions within cells. I will also present ou
r study of disease-causing mutations in TDP-43\, a protein that is often m
utated in amyotrophic lateral sclerosis. The mutations tend to be located
within intrinsically disordered regions\, and I will present the roles of
these regions in fine-tuning the RNA binding properties and functions of t
he protein. Moreover\, I will present our work on the roles that transposa
ble elements play in RNP assembly. I will discuss how these aspects of pro
tein-RNA interactions contribute to regulatory variation\, and thus play i
mportant roles in evolution and disease.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/9
DESCRIPTION:Title: Properties and Functioning of a Developmental Clock\nby Prof.
Dr. Helge Grosshans (Friedrich Miescher Institute for Biomedical Research)
as part of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbst
ract\nThe development of an animal requires proper temporal synchronizatio
n of diverse events\, facilitated by developmental clocks. How such clocks
function is only beginning to emerge. What are their properties? What are
the components that make them run\, and how are they wired? To solve thes
e questions\, we investigate developmental timing in the roundworm C. eleg
ans\, where we can exploit our recent discovery that thousands of genes os
cillate in expression during larval development. Such extensive and robust
molecular clock output\, combined with powerful tools for genetic manipul
ation and screening\, makes C. elegans uniquely suited for dissecting the
underlying clock mechanism. I will report how our work combining genomics\
, genetic and high-throughput single animal-based approaches with theory h
as uncovered a developmental clock with unusual checkpoint properties.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/9/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Giacomo Cavalli (Institute of Human Genetics)
DTSTART:20210115T090000Z
DTEND:20210115T100000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/10
DESCRIPTION:Title: Principles and functional role of 3D genome folding\nby Prof.
Dr. Giacomo Cavalli (Institute of Human Genetics) as part of Colloquium z
ooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe eukaryotic gen
ome folds in 3D in a hierarchy of structures\, including nucleosomes\, chr
omatin fibers\, loops\, chromosomal domains (also called TADs)\, compartme
nts and chromosome territories that are highly organized in order to allow
for stable memory as well as for regulatory plasticity\, depending on int
rinsic and environmental cues. Our lab has provided evidence suggesting th
at the formation of TADs and chromatin loops can assist gene regulation\,
both in Drosophila and in mouse cells. Furthermore\, cellular stress\, suc
h as replicative or oncogene-induced senescence\, can induce a massive nuc
lear reorganization that can affect gene expression. However\, the physica
l nature of compartments\, TADs and loops remain elusive and single-cell s
tudies are critically required to understand it. We characterized chromati
n folding in single cells using super-resolution microscopy\, revealing st
ructural features inaccessible to cell-population analysis. TADs range fro
m condensed and globular objects to stretched conformations. The physical
insulation associated with their borders is variable between individual ce
lls\, yet chromatin intermingling is enriched within TADs compared to adja
cent TADs in a large majority of cells. The spatial segregation of TADs is
further exacerbated during cell differentiation. Favored interactions wit
hin TADs are regulated by cohesin and CTCF through distinct mechanisms. Fu
rthermore\, super-resolution imaging revealed that TADs are subdivided int
o discrete nanodomains. Altogether\, these results provide a physical basi
s for the folding of individual chromosomes at the nanoscale. Our progress
in these fields will be discussed.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/11
DESCRIPTION:Title: New Signal Transduction Targets for Cancer Therapy\nby Prof.
Dr. Tony Hunter (Salk Institute for Biological Studies) as part of Colloqu
ium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nPancreatic du
ctal adenocarcinoma (PDAC) has a dismal prognosis with few treatment optio
ns. We have identified leukemia inhibitory factor (LIF)\, a stem cell fact
or\, as a key paracrine factor\, secreted mainly by activated cancer-assoc
iated-fibroblasts (CAFs) in the tumor micro-environment (TME)\, that acts
on pancreatic tumor cells to maintain a stem cell-like population. Blockad
e of LIF with a neutralizing monoclonal antibody (mAb) slows tumor progres
sion in the KPC mouse model of PDAC and augments efficacy of gemcitabine c
hemotherapy treatment to prolong survival. LIF levels are strongly elevate
d in both mouse and human pancreatic tumor tissue\, and LIF is also is det
ected in serum from tumor-bearing mice and human PDAC patients\, suggestin
g its use as both as a biomarker and as a therapeutic target. In addition
its action on tumor cells\, we have found that LIF acts on myeloid cells i
n the immune microenvironment to sustain a protumorigenic population of tu
mor-associated macrophages.\n\n \n\nHistidine phosphorylation\, the so-cal
led “hidden phosphoproteome”\, is poorly characterized. To study histi
dine phosphorylation we generated mAbs that selectively recognize the 1-pH
is and 3-pHis-isoforms\, and have determined the structural basis of antib
ody recognition of pHis. We have used these mAbs for immunoblotting and im
munofluorescence staining to detect increased levels of pHis proteins in h
uman cell lines\, and also to survey the pHis proteome and identify new si
tes 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 (HC
C) tumor tissue\, as a result of reduced levels of the LHPP pHis phosphata
se in tumor tissue. On this basis\, we propose that LHPP serves as a tumor
suppressor in HCC\, and that histidine phosphorylation can act as a cance
r driver. Consistently\, we have recently observed elevated levels of pHis
proteins in PDAC stromal cells.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/11/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Mitzi Kuroda (Harvard University)
DTSTART:20210201T130000Z
DTEND:20210201T140000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/12
DESCRIPTION:Title: Bivalent Polycomb Complexes as Master Switches of Developmental G
ene Regulation\nby Prof. Dr. Mitzi Kuroda (Harvard University) as part
of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nTh
e genomes of higher organisms are annotated by chromosomal proteins and hi
stone modifications\, which delineate active genes\, regulatory elements\,
and silent regions. This annotation is critical for proper cell type spec
ification\, and an ongoing challenge is to decipher the rules that establi
sh and maintain chromatin organization. Our studies of the highly conserve
d Polycomb group (PcG) epigenetic regulators in Drosophila has led my lab
to propose a model in which the Polycomb Repressive Complex 1 (PRC1) and c
lassical co-activators form ‘bivalent’ protein complexes on transcript
ionally poised developmental genes. We speculate that these function as
‘master switches’ that are responsive to the amount of local acetylati
on or deacetylation activities recruited by cell type specific DNA binding
factors\, leading to stable but reversible activation or repression\, res
pectively. Our model is based on chromatin crosslinking\, affinity purific
ation\, and mass spectrometry experiments\, in which Drosophila PRC1 stron
gly interacts with classical co-activators\, dBRD4 and dMOZ. We are curren
tly exploring potential parallels in mammalian development\n\nOrganizers c
an be contacted at m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoo
m link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/12/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Gregory Gibson (Georgia Institute of Technology)
DTSTART:20210209T130000Z
DTEND:20210209T140000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/13
DESCRIPTION:Title: Transcriptomics for Personalized Medicine\nby Prof. Dr. Grego
ry Gibson (Georgia Institute of Technology) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nTranscriptomics is the st
udy of gene expression. It has enormous potential to understand the molec
ular basis of disease and to help guide therapeutic intervention. These d
ay\, RNA sequencing (scRNAseq) can be used to profile gene expression in t
housands of individual cells\, allowing reserarchers to characterize which
cell types are modified in patients destined to progress to complicated d
isease. 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 disease\, a chronic disease of the gut which is increasing in preval
ence all over the world. Specific genetic signatures predict disease prog
ression\, including the need for colectomy\, and might be used to guide me
dication usage to those in most need or most likely to respond. I will al
so describe a new approach to studying how polygenic risk interacts with e
nvironmental exposures to influence risk of complicated disease.\n\nOrgani
zers can be contacted at m.tariq@lums.edu.pk or 22100032@lums.edu.pk for t
he zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/13/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Susan Wessler (University of California Riverside)
DTSTART:20210224T040000Z
DTEND:20210224T050000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/14
DESCRIPTION:Title: Understanding the strategies evolved by a very successful transpo
sable element\nby Prof. Dr. Susan Wessler (University of California Ri
verside) as part of Colloquium zooming Molecular & Cellular Biology LUMS\n
\n\nAbstract\nTransposable elements (TEs) achieve high copy numbers throug
h waves of amplification called bursts.\nFor a TE to successfully burst it
must be able to significantly increase its copy number without killing it
s\nhost or being silenced by genome surveillance (epigenetic) mechanisms.
However\, because the vast majority of TE\nbursts have been inferred after
the fact – via computational analysis of whole genome sequence – the\
nstealth features they require for success have remained largely undiscove
red. Some features have recently\nbeen discovered by analyzing active burs
ts of the miniature inverted repeat transposable element (MITE)\nmPing and
its autonomous partner Ping in four strains of domesticated rice (Oryza s
ativa\, temperate\njaponica). First\, mPing targets genic regions but avoi
ds exon sequences\, thus minimizing harm to the\nhost. Second\, because mP
ing does not share coding sequences with Ping\, increases in its copy numb
er and\nhost recognition of its sequences do not silence Ping genes\, thus
allowing the continuous production of\nthe proteins necessary to sustain
the burst for decades.\n\nAdditional insights into the mPing burst comes f
rom analyses of an extensive collection of rice genomes\nincluding 3000 do
mesticated strains and a recombinant inbred population. While the survey o
f 3000\nstrains revealed that the burst is very recent and is restricted t
o a few closely related accessions\, analysis\nof the sequences of 272 rec
ombinant inbred lines demonstrated the potential of mPing to rapidly sprea
d\nunimpeded through a large population and increase the frequency of stru
ctural variations.\n\nOrganizers can be contacted at m.tariq@lums.edu.pk o
r 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/15
DESCRIPTION:Title: Genome-wide mapping of protein-DNA interaction dynamics\nby P
rof. Dr. Steve Henikoff (Fred Hutchinson Cancer Research Center) as part o
f Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nWe r
ecently introduced new tools for high-resolution genome-wide chromatin pro
filing and have applied them to study chromatin organization and dynamics
in a variety of model systems\, including yeast\, flies and mammals. Among
the questions addressed are: How do transcription factors find their bind
ing sites in DNA packaged into nucleosomes? How are nucleosomes depleted f
rom gene regulatory regions? What is the relationship between nucleosome d
eposition pathways and chromatin deregulation in disease? Our findings ill
ustrate ways in which chromatin dynamics can play a central role in regula
ting gene expression and silencing.\n\nOrganizers can be contacted at m.ta
riq@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/16
DESCRIPTION:Title: Epigenetic memory over geological timescales\nby Prof. Dr. Hi
ten Madhani (University of California San Francisco) as part of Colloquium
zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nI will describe
our recent work examining the maintenance of DNA methylation in the yeast
Cryptococcus neoformans. In many species\, DNA methylation is established
by a de novo enzyme that can methylate unmethylated DNA. Such enzymes ac
t in narrow developmental windows and this initial activity is subsequentl
y propagated epigenetically via a maintenance enzyme specific for hemimeth
ylated DNA. I will describe a species which lacks a de novo enzyme and on
ly harbors a maintenance enzyme.\n\nOrganizers can be contacted at m.tariq
@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/16/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Denis Duboule (University of Geneva)
DTSTART:20210322T090000Z
DTEND:20210322T100000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/17
DESCRIPTION:Title: Hox gene regulation in embryos and pseudo-embryos\nby Prof. D
r. Denis Duboule (University of Geneva) as part of Colloquium zooming Mole
cular & Cellular Biology LUMS\n\n\nAbstract\nDuring vertebrate development
\, clustered Hox genes are activated in a precise time-sequence\, leading
to patterns necessary to properly establish the body plan. The mechanism u
nderlying this in cis timing phenomenon has remained unknown ever since it
s observation in 1989\, due to the difficulty to approach it using early g
astrulating mouse embryos. I will discuss an alternative possibility\, whi
ch is to use pseudo-embryos produced out of ES cells (referred to as gastr
uloids) to address this now 30 years old question and will show some preli
minary data indicating that this system may allow us to more efficiently t
ackle this issue in the next few years to come.\n\nOrganizers can be conta
cted at m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/17/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Wendi Bickmore (University of Edinburgh)
DTSTART:20210407T100000Z
DTEND:20210407T110000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/18
DESCRIPTION:Title: The role of spatial proximity in genome regulation\nby Prof.
Dr. Wendi Bickmore (University of Edinburgh) as part of Colloquium zooming
Molecular & Cellular Biology LUMS\n\n\nAbstract\nImaging and genomic tech
nologies have opened up large-scale interrogation of 3D genome organisatio
n in the cell nucleus. This has revealed multiple layers of organisation a
nd at different scales\, including distal interactions of genome compartme
nts\, topologically associating domains (TADs) and specific cis interactio
ns between either active or repressive elements. Progress is being made to
ward understanding the molecular mechanisms that mediate these layers of o
rganisation. However\, understanding the functional significance of 3D org
anisation across genomic scales lags behind. To what extent does 3D organi
sation drive genome regulation\, or are some aspects of 3D organisation si
mply an emergent property of genome and protein functions? In this talk I
will describe our efforts to determine the functional significance of the
3D genome – from the action of polycomb complexes in bridging distal int
eractions between repressed loci\, to the role of TADs and enhancer-promot
er proximity in enhancer-driven gene activation.\n\nOrganizers can be cont
acted at m.tariq@lums.edu.pk or 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/19
DESCRIPTION:Title: Finding your place: Transcription factors as sensors and modifier
s of chromatin\nby Prof. Dr. Dirk Schubeler (Friedrich Miescher Instit
ute for Biomedical Research) as part of Colloquium zooming Molecular & Cel
lular Biology LUMS\n\n\nAbstract\nTranscription factors only bind a minori
ty of their motifs in large mammalian genomes. One potential explanation i
s that many motifs are not accessible for binding due to the action of chr
omatin and DNA methylation. We are using mammalian stem cell models to und
erstand this important interplay between gene regulation\, chromatin struc
ture and DNA methylation. We study the dynamics of the epigenome and test
regulatory models in cellular models by genetic perturbation and genome ed
iting approaches. I will discuss our recent efforts in understanding how t
he sensitivity to DNA methylation can limit transcription factor binding i
n the context of the cell\, the identification of a novel\, strong activat
ing factor and how transcripton factors rely on specific chromatin remodel
ers 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://stable.researchseminars.org/talk/MCB_LUMS/19/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Robert Weinberg (Massachusetts Institute of Technology)
DTSTART:20210311T140000Z
DTEND:20210311T150000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/20
DESCRIPTION:Title: Mechanisms of the Malignant Progression of Carcinomas\nby Pro
f. Dr. Robert Weinberg (Massachusetts Institute of Technology) as part of
Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe fo
rmation of primary tumors depends in no small part on the acquisition by e
volving primary tumor cells of a series of somatically mutated alleles. H
owever\, the last step of tumor progression involves the processes of inva
sion and metastasis and it has been less clear precisely how these traits
are acquired. As will be described\, these phenotypes of high-grade malign
ancy are consequences of the actions of non-genetic\, i.e\,\, epigenetic c
hanges in cancer cells that are mediated by induction of the cell-biologic
al program termed the epithelial-mesenchymal transition\, which confers ma
ny of the traits that are associated traditionally with the changes associ
ated with the carcinoma cells of high-grade tumors. In addition\, inductio
n of this program is associated with the acquisition of stemness\, that is
\, tumor-initiating potential\, which is essential for successful metastas
is formation. These various non-genetic processes will be discussed!\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/20/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Shiv Grewal (National Institutes of Health)
DTSTART:20210526T120000Z
DTEND:20210526T130000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/21
DESCRIPTION:Title: Epigenetic genome control by RNA-based mechanisms\nby Prof. D
r. Shiv Grewal (National Institutes of Health) as part of Colloquium zoomi
ng Molecular & Cellular Biology LUMS\n\n\nAbstract\nGenome-wide sequencing
of the human genome and several model organisms has greatly facilitated r
esearch into genome structure and function. Much attention is now focused
on understanding how the functional organization of the genome supports t
ranslation of genetic information into formation of different cell types d
uring development\, and how it contributes to disease progression. We hav
e shown previously that distinct histone methylation patterns organize chr
omosomes into “open” euchromatin (H3K4me) and “closed” heterochrom
atin (H3K9me) domains\, to modulate use of the genome. Our work has also
revealed that heterochromatin can be targeted by RNAi machinery and/or by
pathways requiring RNA elimination and transcription termination factors.
Moreover\, we find that RNA processing factors and heterochromatin machin
ery are part of an adaptive cellular mechanisms that can reprogram the gen
ome in response to changes in environmental growth conditions and developm
ental signals. Our most recent work on the assembly and epigenetic inheri
tance of silenced chromatin domains\, essential for proper gene regulation
during development will be presented.\n\nThe organizers can be contacted
at 22100032@lums.edu.pk for the zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/21/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Ellen Rothenberg (California Institute of Technology)
DTSTART:20210624T040000Z
DTEND:20210624T060000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/22
DESCRIPTION:Title: Gene network and epigenetic mechanisms controlling the generation
of T lymphocytes\nby Prof. Dr. Ellen Rothenberg (California Institute
of Technology) as part of Colloquium zooming Molecular & Cellular Biology
LUMS\n\n\nAbstract\nT lymphocytes are vital components of the immune syst
em in humans and other mammals. They are generated by multiple waves of b
lood cell precursors that migrate from the bone marrow to a special organ\
, the thymus\, where the stem cell-like precursor cells encounter signals
that cause them to differentiate into T cells. This process is important f
or health by providing resistance to infection and cancer\, and it is also
very illuminating as a model system to show how environmental signaling\,
endogenously expressed transcription factors\, and epigenetic chromatin c
hanges can work together in an orderly\, stepwise process to convert cells
efficiently from stem-like cells to effective\, useful differentiated cel
ls. We can “zoom in” to observe and dissect this process through powe
rful in vitro culture systems that mimic the thymus in an open format\, wh
ich allows the developing cells to be observed and manipulated. \nThe Rot
henberg lab has focused on answering three kinds of questions. First\, how
do the transcription factors in these cells act in a cascade\, so that ea
ch transcription factor works to activate or shut off other transcription
factors in an orderly way\, which then themselves change the expression of
another set of genes? Second\, how does the epigenetic state of the chro
matin affect what these transcription factors can do at a given stage\, an
d how do the factors themselves alter the epigenetic state to allow differ
entiation to proceed? Third\, how do these mechanisms explain the high eff
iciency but slow speed of this developmental process? The talk will show
how recent results shed light on these questions.\n\nOrganizers can be con
tacted at 22100032@lums.edu.pk for the Zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/22/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Mariana Wolfner (Cornell University)
DTSTART:20211005T130000Z
DTEND:20211005T143000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/23
DESCRIPTION:Title: Activating eggs and stimulating reproduction: the molecular view
from Drosophila (and beyond).\nby Prof. Dr. Mariana Wolfner (Cornell U
niversity) as part of Colloquium zooming Molecular & Cellular Biology LUMS
\n\n\nAbstract\nSuccessful reproduction in internal-fertilizing animals re
quires molecular modification of both the oocyte and the female. Oocytes m
ust “activate”\, transitioning from meiotic and molecular arrest to th
e totipotency of early embryogenesis after fertilization. The female’s p
hysiology must change to support her reproductive success\, egg production
\, and her progeny. Versions of these phenomena are universal\, including
in human fertility and that of insect vectors of diseases like Dengue and
Zika. But they can be particularly well dissected using model-organisms su
ch as Drosophila fruit flies. This talk will present results from studies
using this model to dissect mechanisms that activate eggs\, and others to
elucidate 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 embryogenesis. We will then consider how the female’s physiological s
tate is modified by seminal proteins that she receives during mating\, and
how these male-derived proteins act to stimulate her egg production\, inc
luding a signal that activates her eggs. The talk will conclude by summari
zing how these findings inform our understanding of mechanisms of egg acti
vation and seminal protein actions in animals more generally.\n\nOrganizer
s can be reached out at 22100032@lums.edu.pk for the Zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/23/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. David Baulcombe (Cambridge University)
DTSTART:20211013T090000Z
DTEND:20211013T103000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/24
DESCRIPTION:Title: RNA silencing\, disease resistance and non-Mendelian inheritance<
/a>\nby Prof. Dr. David Baulcombe (Cambridge University) as part of Colloq
uium zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nRNA silencin
g was discovered by accident as a virus defense mechanism but our current
understanding is that it is a family of related mechanisms affecting trans
posons and gene expression. In this talk I will describe how\, in defense\
, RNA silencing is relevant as more than protection against viruses – it
influences resistance against cellular as well as viral pathogens and it
operates as part of a network of mechanisms in which the different layers
of the plants innate immune system are connected and integrated. I will al
so describe how RNA silencing can influence non-Mendelian inheritance patt
erns of gene expression in the progeny of crosses between genetically dist
inct parents.\n\nOrganizers can be contacted at 22100032@lums.edu.pk for t
he Zoom link.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/24/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Gregory Hannon (Cambridge University)
DTSTART:20211119T110000Z
DTEND:20211119T123000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/25
DESCRIPTION:Title: A small RNA-based innate immune system guards the integrity of ge
rm cell genomes\nby Prof. Dr. Gregory Hannon (Cambridge University) as
part of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstrac
t\nPIWI-family proteins and their associated small RNAs (piRNAs) act in an
evolutionarily conserved innate immune mechanism that provides an essenti
al protection for germ cell genomes against the activity of mobile genetic
elements. piRNA populations comprise a molecular definition of transposon
s that permits them to be distinguished from host genes and selectively si
lenced. piRNAs can be generated in two distinct ways. Primary piRNAs emana
te from discrete genomic loci\, termed piRNA clusters\, and appear to be d
erived from long\, single-stranded precursors. The biogenesis of primary p
iRNAs involves at least two nucleolytic steps. Zucchini cleaves piRNA clus
ter transcripts to generate monophosphorylated piRNA 5’ ends. piRNA 3’
ends are likely formed by exonucleolytic trimming\, after a piRNA precurs
or is loaded into its PIWI partner. Secondary piRNAs arise during the adap
tive ping-pong cycle\, with their 5’ termini being formed by the activit
y of PIWIs themselves. At least in Drosophila\, piRNAs are maternally depo
sited and transmit an epigenetic signal essential for the effective contro
l of at least some transposable elements. Our continuing efforts combine g
enetics\, biochemistry\, structural biology\, and evolutionary and computa
tional approaches to understand how the piRNA pathway effectively discrimi
nates self from non-self at the genomic level.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/25/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Norbert Perrimon (Harvard University)
DTSTART:20220325T140000Z
DTEND:20220325T150000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/26
DESCRIPTION:Title: Inter-organ communication: Studies in Drosophila\nby Prof. Dr
. Norbert Perrimon (Harvard University) as part of Colloquium zooming Mole
cular & Cellular Biology LUMS\n\n\nAbstract\nI will discuss our ongoing st
udies to identify and characterize communication pathways between major or
gans in Drosophila. Organ-to-organ communications are critical to living s
ystems and play major roles in homeostasis. For example\, the vertebrate C
NS receives information regarding the status of peripheral metabolic proce
sses via hormonal signaling and direct macromolecular sensing. In addition
\, skeletal muscles produce various myokines that influence metabolic home
ostasis\, lifespan\, and the progression of age-related diseases and aging
in non-muscle tissues. Using genetic screening\, transcriptome analyses
and proteomic approaches\, we are identifying and characterizing secreted
factors by which organs communicate their physiological state to others in
both homeostasis and altered metabolism\, as well as tumor models. These
studies are providing fundamental insights into how biological processes o
bserved in one tissue/organ (e.g.\, decreased cellular metabolism\, mitoch
ondrial dysfunction) influence the state of other tissues/organs.\n
LOCATION:https://stable.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:20260404T094600Z
UID:MCB_LUMS/27
DESCRIPTION:Title: Deconstructing the principles of cellular hierarchy in tumors wit
h a developmental origin\nby Prof. Dr. Cedric Maurange (Institute of D
evelopmental Biology of Marseilles) as part of Colloquium zooming Molecula
r & Cellular Biology LUMS\n\n\nAbstract\nPediatric cancers are different f
rom adult cancers in that they carry much fewer genetic lesions but are ab
le to progress extremely rapidly. In addition\, brain cancers are over-rep
resented in children. Recent data has demonstrated that pediatric brain ca
ncers often originate during embryonic and fatal stages\, and aberrantly r
ecapitulate sub-parts of developmental programs. It has been proposed that
such tumors are « locked » into perpetual development. Yet it is often
unclear why these developmental programs become mis-regulated during the c
ourse of development and how they are coopted to promote tumorigenesis. We
are addressing these questions using a Drosophila model of neural tumors
with a developmental origin\, resembling in many aspect pediatric cancers
in human. Our work has identified the coopted developmental program that s
ustains tumor growth and has deciphered their hierarchical cellular organi
zation. During my talk\, I will present our recent finding that epigenetic
regulators of the PRC2 and MLL1/2-COMPASS complexes regulate this hierarc
hy\, and how their inactivation can trigger plasticity and cancer stem cel
l heterogeneity.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/27/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Danny Reinberg (New York University)
DTSTART:20220621T130000Z
DTEND:20220621T140000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/28
DESCRIPTION:Title: Polycomb\, Inheritance and Disease\nby Prof. Dr. Danny Reinbe
rg (New York University) as part of Colloquium zooming Molecular & Cellula
r Biology LUMS\n\n\nAbstract\nEpigenetics encompasses changes in gene expr
ession profiles that occur without alterations in the genomic DNA sequence
of a cell. This arises from the dynamic processes that structure regions
of chromosomal DNA through a range of compaction in eukaryotes. The altere
d pattern of gene expression is pivotal to cellular differentiation and de
velopment and is inherited by daughter cells thereby maintaining the integ
rity\, specifications\, and functions for a given cell type. Aberrancies i
n this epigenetic process give rise to perturbations that are also inherit
ed and disruptive to normal cellular properties.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/28/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Monica P. Colaiacovo (Harvard Medical School)
DTSTART:20221109T140000Z
DTEND:20221109T150000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/29
DESCRIPTION:Title: Location and numbers: how recombination and our chemical landscap
e converge on meiosis\nby Prof. Dr. Monica P. Colaiacovo (Harvard Medi
cal School) as part of Colloquium zooming Molecular & Cellular Biology LUM
S\n\n\nAbstract\nResearch in our laboratory is focused on understanding th
e regulation of mechanisms that promote accurate chromosome segregation du
ring meiosis\, such as recombination\, and how exposure to endocrine-disru
pting chemicals (EDCs) affect these mechanisms. Errors in achieving accura
te chromosome segregation during meiosis can result in the formation of an
euploid gametes (i.e.\, eggs and sperm carrying an incorrect number of chr
omosomes)\, which is associated with miscarriages\, stillbirths\, infertil
ity\, and birth defects. Our team has directly demonstrated in a metazoan
(the nematode C. elegans) how the position of DNA double-strand breaks and
crossover recombination events are critical for accurate chromosome segre
gation and how exposure to an abundantly used plasticizer (DEHP) alters th
is regulation. Ongoing studies are examining what factors regulate the dis
tribution of recombination events and how other EDCs differentially affect
female and male meiosis\, leading to embryonic lethality and infertility.
\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/29/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Dietrich M. Egli (Columbia University)
DTSTART:20221110T080000Z
DTEND:20221110T090000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/30
DESCRIPTION:Title: Genome stability in embryonic development and reprogramming\n
by Prof. Dr. Dietrich M. Egli (Columbia University) as part of Colloquium
zooming Molecular & Cellular Biology LUMS\n\n\nAbstract\nThe events occurr
ing in the beginning of human development are highly consequential for eve
rything that follows\, but remain poorly understood and little investigate
d. Most human embryos fail to develop shortly after fertilization. This in
efficiency in development is primarily caused by an unstable genome\, resu
lting in aneuploidies\, DNA damage\, cell cycle arrest\, and in developing
embryos likely novel mutations. I will present our novel insight on how t
he embryo replicates its DNA and how inefficiencies in DNA repair in the e
mbryo shape fertility as well as our health throughout life.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/30/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Fred Winston (Harvard Medical School)
DTSTART:20230203T130000Z
DTEND:20230203T140000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/31
DESCRIPTION:Title: Analysis of factors that control transcriptional fidelity and chr
omatin structure\nby Prof. Dr. Fred Winston (Harvard Medical School) a
s part of Colloquium zooming Molecular & Cellular Biology LUMS\n\n\nAbstra
ct\nNucleosomes are barriers for transcription. To help to alleviate these
barriers\, a class of factors called histone chaperones modulates histone
-DNA interactions. Our work has focused on set of three histone chaperones
that are essential for viability and that are conserved from yeast to hum
ans. Our studies\, using S. cerevisiae as a model system\, have shown that
these three factors\, Spt6\, Spn1\, and FACT\, are broadly required for t
he fidelity of transcription and the integrity of chromatin structure. Whi
le all three histone chaperones are vital for growth\, we have found unexp
ected connections between their functions that suggest that they interact
in a network that is critical for their functions in transcription\, as we
ll as other chromatin-templated functions including DNA replication and ge
nome stability.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/31/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Sue Biggins (Fred Huch Cancer Center)
DTSTART:20230306T150000Z
DTEND:20230306T160000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/32
DESCRIPTION:Title: How do cells inherit the right chromosomes?\nby Prof. Dr. Sue
Biggins (Fred Huch Cancer Center) as part of Colloquium zooming Molecular
& Cellular Biology LUMS\n\n\nAbstract\nThe precise regulation of cell div
ision is critical to processes such as self-renewal\, proliferation and de
velopment. A key event in the cell cycle is the partitioning of every pair
of duplicated chromosomes to daughter cells. Chromosomes segregate using
their kinetochores\, the specialized protein structures that are assembled
on centromeric DNA sequences and attach to spindle microtubules. I will
discuss our recent advances in isolating and reconstituting kinetochores a
nd studying their behavior by biochemical and biophysical techniques in vi
tro. This 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 wh
at it has revealed about the centromeric nucleosome and the specificity of
the centromeric DNA\, work that ultimately is critical to understanding h
ow cells maintain genomic stability.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/32/
END:VEVENT
BEGIN:VEVENT
SUMMARY:Prof. Dr. Constance Cepko (Harvard Stem Cell Institute)
DTSTART:20230329T103000Z
DTEND:20230329T113000Z
DTSTAMP:20260404T094600Z
UID:MCB_LUMS/33
DESCRIPTION:Title: Gene Therapy to Prolong Vision\nby Prof. Dr. Constance Cepko
(Harvard Stem Cell Institute) as part of Colloquium zooming Molecular & Ce
llular Biology LUMS\n\n\nAbstract\nThere are >200 human disease genes lead
ing to blindness. Although gene therapy in which each disease gene is augm
ented or edited is possible\, this approach would be extremely expensive a
nd logistically challenging. To provide an alternative\, more general appr
oach\, our laboratory has been analyzing mouse models of blindness\, looki
ng for problems that are common across genotypes. We were particularly int
erested in mouse models for retinitis pigmentosa (RP)\, as it is well mode
led in mice\, relative to humans. In RP\, the disease starts with the expr
ession of mutant genes in rod photoreceptors\, the cell type that initiate
s dim light vision\, leading to poor night vision. However\, color vision\
, which originates with cone photoreceptors\, is normal at birth. Over tim
e\, cones become affected due to bystander effects from rod loss. This cau
ses color blindness and can lead to total blindness. Other cells also are
affected by the loss of rods: the retinal pigmented epithelial cells (RPE)
\, which provide various types of support to rods and cones. Studies of th
ese mouse models led to the hypothesis that the bystander effects include:
oxidative damage\, metabolic shortcomings\, and inflammation. To combat t
hese problems\, many different types of genes were delivered using adeno-a
ssociated viruses (AAV). Genes that fight inflammation\, a transcription f
actor that regulates genes that fight oxidative damage\, and genes that pr
ovide metabolic support were found to prolong cone and RPE survival as wel
l as vision across 3 strains of RP mice.\n
LOCATION:https://stable.researchseminars.org/talk/MCB_LUMS/33/
END:VEVENT
END:VCALENDAR