MELIKE CANSEL EREN +905458536377| erenmelikecansel@gmail.com Izmir
Turkey Education Uskudar University
M.Sc. September 2019-June
2022 Istanbul
Turkey Cumulative GPA:3.78 High Honor Student Master Science in Neuroscience Department of Neuroscience Sciences Thesis: Investigation of TopoII ß Gene Expression in LPS-Induced HMC3 Microglia Cell Line Pamukkale University
B.Sc. September2015-June 2019 Denizli
Turkey Cumulative GPA: 3.0 Honour Student Bachelor of Science in Physical Therapy and Rehabilitation Universitat de Barcelona September2018- June 2019 Barcelona
Spain International Student ERASMUS Study Abroad Program Worked in the multiple sclerosis (MS) clinic
where each patient was treated using a biopsychosocial model. Collaborated with physicians
physiotherapists
and psychologists to evaluate patients and provide education about the disease and its progression to patients and their families. Assisted in assessing therapy and treatment processes. Coordinated the association for the solidarity of MS patients and their relatives. Conducted ergonomic assessments of patients' homes and workplaces to optimize their participation in daily life. Facilitated patients' re- occupation. • Worked in the Parkinson's disease (PD) clinic
following a biopsychosocial model for patient treatment. Collaborated with physicians
physiotherapists
and psychologists to evaluate patients and provide weekly education about the disease and its course to patients and their families. Assisted in assessing therapy and treatment processes. Coordinated the association for the solidarity of PD patients and their relatives. Conducted ergonomic assessments of patients' homes and workplaces to optimize their participation in daily life. Facilitated patients' return to home settings. Skills & Qualifications • Ability to work independently and efficiently. • Strong organizational and task prioritization skills. • Excellent communication skills and proficiency in performing administrative and clerical tasks. • Proficient in general laboratory procedures
techniques
and documentation. • Willingness to learn and adapt to new techniques and technologies. • Fluent in English
Spanish
French
and Catalan. • Proficient in statistical analysis and software such as SPSS
MATLAB
and Python. • Proficient in using various software programs
including Microsoft Office Suite (Word
Excel
PowerPoint). • Advanced knowledge and experience in 3D cell culture techniques. • Skilled in protein isolation
Western Blot
PCR
rt-qPCR
toxicity testing
IHC
Northern Blot
and ELISA. • Proficient in anatomical dissection studies for medical and veterinary purposes. • Experienced in static analysis of behavioral data and microarray data. • Familiarity with electrophysiology
imaging
protein purification
and optical and electron microscopy techniques. • Advanced level proficiency in conducting animal experiments
behavioral experiments
anatomical dissection
and molecular analysis.From Astrocytes to Autism Our laboratory is interested in the genetics and genomics of behavior in health and disease. We utilize a variety of techniques
including human molecular genetics
informatics
mouse behavior
in vitro and in vivo neuroscience
and neuroanatomy. We are continuously developing novel methods for transgenesis
gene manipulation
and transcriptional profiling of the brain. These tools help us to develop mouse models for discovery and modeling of genetic variations based on human patient populations
in order to understand the cellular and molecular underpinnings of behavior. We are particularly focused on neurodevelopmental conditions
including the autism spectrum. We study intellectual and developmental syndromes to better understand how gene expression differences can change the trajectory of neural development. We believe that a better understanding of the basic science behind syndromic conditions has the potential to give patients and families more agency and options in addressing their unique challenges. We also are very interested to understand and be informed by the needs of the families themselves
and welcome engagement with the community of the syndromes we work on. Our specific applications of these methods currently span six different
inter-related areas of research: Transcriptional and translational regulation
and its dysregulation in neuropsychiatric and neurodevelopmental conditions: Impacts of genetic variation. Genetic variants
both those common in the population and those which are de novo—which are variations not seen in the parents but found in an offspring
due to e.g. spontaneous mutations in germ cells—have been associated with neuropsychiatric diseases by way of genome-wide association studies and genomic analysis of parent-child trios
respectively. In both cases
a vast number of the variations associated with or unique to disease fall in non-protein coding DNA
making it difficult to discern whether and how a variation begets disease. Using Massively Parallel Reporter Assays (MPRAs)
we can systematically assess the effects of large sets of variants falling in a) untranslated mRNA elements
as well as b) noncoding variants falling in putative regulatory regions. We are also using this technology to explore putative transcriptional regulators of CNS cell types
sex differences in enhancer element usage
potential antisense oligo (ASO) therapy for use in treating intellectual and developmental disability
and the effects of non-coding variants on translation and mRNA stability. We also have been performing ongoing computational genomic analysis in collaboration with the Simons Simplex Consortium
examining mutational burdens and their potential functions in family cohorts with a child suffering from ASD. Local and conditional translation of mRNA. Neurons have been long known to localize certain mRNAs to their axons
dendrites
and synapses for translation at the site of use. Our lab was the first to definitively show and characterize this process in astrocytes
another abundant brain cell type
and microglia
an immune cell of the brain. Using similar techniques
including Translating Ribosome Affinity Purification (TRAP) and Ribosome Footprinting (RF)
we are continuing to characterize the mechanisms regulating RNA localization and translation in glial cell types and specific neuronal populations. Moreover
these methods enable us to look at e.g. effects of neuronal stimulation on mRNA occupancy
providing potential insights into mechanisms of conditional translation. Finally
using technologies such as CLIP-seq (an RNA analogue of ChIP seq)
one can identify RNA binding proteins and their genes
providing another means of insight into regulation of RNA location and translation. Longitudinal transcriptional signatures that underlie individual variance and neuronal disorder phenotypes. Currently available transcriptional tools are limited in that they only provide a one-dimensional snapshot in time – the molecular signature of the brain at the moment of harvest. We sought to overcome this limitation by developing in vivo Calling Cards
a tool that permanently records transient protein-DNA interactions
that builds on a technology pioneered by our collaborators
the Mitra Lab. We further adapted the tool to be compatible with standard single cell technologies
allowing us to assay gene expression and transcription factor binding with single cell resolution. Calling Cards has opened the door to multiple avenues of investigation: characterizing potentially aberrant molecular signatures in models of neurodevelopmental conditions
adapting our technology to only record during specified time windows
and identifying how early-life transcriptional changes can underpin later-life susceptibility or resilience. Genetic and behavioral mouse models of neurodevelopmental conditions and risk factors : Genetic factors. While one type of genetic variation
discussed above
does not directly impact the protein-coding genome
some variations are capable of compromising one or multiple proteins
especially in the cases of chromosomal mutations and transcriptional factor mutations. In these cases
a gene or a set of genes become implicitly responsible for the observed phenotypes
which makes the disease amenable to modeling by use of gene knockout mice. With the expertise from characterizing mouse models of William Syndrome (a disease that features hypersociability
in interesting contrast to ASDs)
our lab continues this journey by focusing on a neurodevelopmental disorder (NDD) related gene
Myelin Transcription Factor 1 Like (MYT1L). Utilizing the MYT1L haploinsufficiency mouse model mimicking a patient mutation
we are seeking to understand how MYT1L mutations lead to various human patient phenotypes from molecular
to cellular
and to circuitry levels. This project leverages a wide range of techniques we established in the lab
including RNA-seq
ATAC-seq
CUT&RUN
MPRA
Calling Card
electrophysiology
and behavioral paradigms. Furthermore
we generated MYT1L conditional knockout (cKO) and conditional rescue mouse lines to investigate cell-type/development specific functions of MYT1L and explore therapeutic opportunities for MYT1L Syndrome. Sex differences. Almost all neuropsychiatric diseases appear to carry uneven incidence among males and females—for example
ASC
ADHD
and schizophrenia are diagnosed more in men
while depression
anxiety
and PTSD tend to affect more women. Animal research
as both a behavioral model and a living experimental model of the nervous system
has until recently—and often still does—only performed experiments in male animals. This has left huge gaps in knowledge about whether and how sex affects behavior
neuroanatomy
and gene expression. We have characterized and are continuing to explore the genetic and hormonal mechanisms of sex differences
specifically in depression and autism. Environmental factors. Many neurotransmitter and neuromodulator systems targeted by drugs play vital roles in neurodevelopment
and disruption of these systems during critical periods of brain development can have lasting impacts on behavioral circuits. To understand the potential impact of changes to the serotonergic system during neurodevelopment on later behavioral function
we investigated the role of in utero exposure to selective serotonin reuptake inhibitors (SSRI
a class of antidepressant) on social and sensory behaviors
which are often impacted in intellectual and developmental disabilities. We found that this early targeting of the serotonin system resulted in reduced early social communication
altered social hierarchy behaviors
and increased sensitivity to tactile stimulation. We then took the strategies developed to understand SSRI exposure and applied them to develop a model of Neonatal Opioid Withdrawal Syndrome to understand the impact of clinically-relevant continued postnatal opioid maintenance and mitigation strategies on long-term behavioral function. This collaborative effort with the Al-Hasani Lab revealed that ontogenetic exposure to oxycodone disrupts weight trajectories
early communicative behavior and early somatosensory reflexes in offspring
as well as sex-specific changes in sensory and reward processing.