---
_id: '13107'
abstract:
- lang: eng
  text: "Within the human body, the brain exhibits the highest rate of energy consumption
    amongst all organs, with the majority of generated ATP being utilized to sustain
    neuronal activity. Therefore, the metabolism of the mature cerebral cortex is
    geared towards preserving metabolic homeostasis whilst generating significant
    amounts of energy. This requires a precise interplay between diverse metabolic
    pathways, spanning from a tissue-wide scale to the level of individual neurons.
    Disturbances to this delicate metabolic equilibrium, such as those resulting from
    maternal malnutrition\r\nor mutations affecting metabolic enzymes, often result
    in neuropathological variants of neurodevelopment. For instance, mutations in
    SLC7A5, a transporter of metabolically essential large neutral amino acids (LNAAs),
    have been associated with autism and microcephaly. However, despite recent progress
    in the field, the extent of metabolic restructuring that occurs within the developing
    brain and the corresponding alterations in nutrient demands during various critical
    periods remain largely unknown. To investigate this, we performed metabolomic
    profiling of the murine cerebral cortex to characterize the metabolic state of
    the forebrain at different developmental stages. We found that the developing
    cortex undergoes substantial metabolic reprogramming, with specific sets of metabolites
    displaying stage-specific changes. According to our observations, we determined
    a distinct temporal period in postnatal development during which the cortex displays
    heightened reliance on LNAAs. Hence, using a conditional knock-out mouse model,
    we deleted Slc7a5 in neural cells, allowing us to monitor the impact of a perturbed
    neuronal metabolic state across multiple developmental stages of corticogenesis.
    We found that manipulating the levels of essential LNAAs in cortical neurons in
    vivo affects one particular perinatal developmental period critical for cortical
    network refinement. Abnormally low intracellular LNAA levels result in cell-autonomous
    alterations in neuronal lipid metabolism, excitability, and survival during this
    particular time window. Although most of the effects of Slc7a5 deletion on neuronal
    physiology are transient, derailment of these processes during this brief but
    crucial window leads to long-term circuit dysfunction in mice. In conclusion,
    out data indicate that the cerebral cortex undergoes significant metabolic reorganization
    during development. This process involves the intricate integration of multiple
    metabolic pathways to ensure optimal neuronal function throughout different developmental
    stages. Our findings offer a paradigm for understanding how neurons synchronize
    the expression of nutrient-related genes with their activity to allow proper brain
    maturation. Further, our results demonstrate that disruptions in these precisely
    calibrated metabolic processes during critical periods of brain development may
    result in neuropathological outcomes in mice and in humans."
acknowledged_ssus:
- _id: PreCl
- _id: Bio
- _id: EM-Fac
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Lisa
  full_name: Knaus, Lisa
  id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
  last_name: Knaus
citation:
  ama: 'Knaus L. The metabolism of the developing brain : How large neutral amino
    acids modulate perinatal neuronal excitability and survival. 2023. doi:<a href="https://doi.org/10.15479/at:ista:13107">10.15479/at:ista:13107</a>'
  apa: 'Knaus, L. (2023). <i>The metabolism of the developing brain : How large neutral
    amino acids modulate perinatal neuronal excitability and survival</i>. Institute
    of Science and Technology Austria. <a href="https://doi.org/10.15479/at:ista:13107">https://doi.org/10.15479/at:ista:13107</a>'
  chicago: 'Knaus, Lisa. “The Metabolism of the Developing Brain : How Large Neutral
    Amino Acids Modulate Perinatal Neuronal Excitability and Survival.” Institute
    of Science and Technology Austria, 2023. <a href="https://doi.org/10.15479/at:ista:13107">https://doi.org/10.15479/at:ista:13107</a>.'
  ieee: 'L. Knaus, “The metabolism of the developing brain : How large neutral amino
    acids modulate perinatal neuronal excitability and survival,” Institute of Science
    and Technology Austria, 2023.'
  ista: 'Knaus L. 2023. The metabolism of the developing brain : How large neutral
    amino acids modulate perinatal neuronal excitability and survival. Institute of
    Science and Technology Austria.'
  mla: 'Knaus, Lisa. <i>The Metabolism of the Developing Brain : How Large Neutral
    Amino Acids Modulate Perinatal Neuronal Excitability and Survival</i>. Institute
    of Science and Technology Austria, 2023, doi:<a href="https://doi.org/10.15479/at:ista:13107">10.15479/at:ista:13107</a>.'
  short: 'L. Knaus, The Metabolism of the Developing Brain : How Large Neutral Amino
    Acids Modulate Perinatal Neuronal Excitability and Survival, Institute of Science
    and Technology Austria, 2023.'
date_created: 2023-06-01T09:05:24Z
date_published: 2023-05-31T00:00:00Z
date_updated: 2024-02-07T08:03:33Z
day: '31'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: GaNo
doi: 10.15479/at:ista:13107
ec_funded: 1
file:
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language:
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month: '05'
oa: 1
oa_version: Published Version
page: '147'
project:
- _id: 25444568-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715508'
  name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
    and in vitro Models
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: W1232-B24
  name: Molecular Drug Targets
publication_identifier:
  issn:
  - 2663 - 337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
  record:
  - id: '12802'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
title: 'The metabolism of the developing brain : How large neutral amino acids modulate
  perinatal neuronal excitability and survival'
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2023'
...
---
_id: '12364'
abstract:
- lang: eng
  text: "Autism spectrum disorders (ASDs) are a group of neurodevelopmental disorders
    character\x02ized by behavioral symptoms such as problems in social communication
    and interaction, as\r\nwell as repetitive, restricted behaviors and interests.
    These disorders show a high degree\r\nof heritability and hundreds of risk genes
    have been identifed using high throughput\r\nsequencing technologies. This genetic
    heterogeneity has hampered eforts in understanding\r\nthe pathogenesis of ASD
    but at the same time given rise to the concept of convergent\r\nmechanisms. Previous
    studies have identifed that risk genes for ASD broadly converge\r\nonto specifc
    functional categories with transcriptional regulation being one of the biggest\r\ngroups.
    In this thesis, I focus on this subgroup of genes and investigate the gene regulatory\r\nconsequences
    of some of them in the context of neurodevelopment.\r\nFirst, we showed that mutations
    in the ASD and intellectual disability risk gene Setd5 lead\r\nto perturbations
    of gene regulatory programs in early cell fate specifcation. In addition,\r\nadult
    animals display abnormal learning behavior which is mirrored at the transcriptional\r\nlevel
    by altered activity dependent regulation of postsynaptic gene expression. Lastly,\r\nwe
    link the regulatory function of Setd5 to its interaction with the Paf1 and the
    NCoR\r\ncomplex.\r\nSecond, by modeling the heterozygous loss of the top ASD gene
    CHD8 in human cerebral\r\norganoids we demonstrate profound changes in the developmental
    trajectories of both\r\ninhibitory and excitatory neurons using single cell RNA-sequencing.
    While the former\r\nwere generated earlier in CHD8+/- organoids, the generation
    of the latter was shifted to\r\nlater times in favor of a prolonged progenitor
    expansion phase and ultimately increased\r\norganoid size.\r\nFinally, by modeling
    heterozygous mutations for four ASD associated chromatin modifers,\r\nASH1L, KDM6B,
    KMT5B, and SETD5 in human cortical spheroids we show evidence of\r\nregulatory
    convergence across three of those genes. We observe a shift from dorsal cortical\r\nexcitatory
    neuron fates towards partially ventralized cell types resembling cells from the\r\nlateral
    ganglionic eminence. As this project is still ongoing at the time of writing,
    future\r\nexperiments will aim at elucidating the regulatory mechanisms underlying
    this shift with\r\nthe aim of linking these three ASD risk genes through biological
    convergence."
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Christoph
  full_name: Dotter, Christoph
  id: 4C66542E-F248-11E8-B48F-1D18A9856A87
  last_name: Dotter
  orcid: 0000-0002-9033-9096
citation:
  ama: Dotter C. Transcriptional consequences of mutations in genes associated with
    Autism Spectrum Disorder. 2022. doi:<a href="https://doi.org/10.15479/at:ista:12094">10.15479/at:ista:12094</a>
  apa: Dotter, C. (2022). <i>Transcriptional consequences of mutations in genes associated
    with Autism Spectrum Disorder</i>. Institute of Science and Technology Austria.
    <a href="https://doi.org/10.15479/at:ista:12094">https://doi.org/10.15479/at:ista:12094</a>
  chicago: Dotter, Christoph. “Transcriptional Consequences of Mutations in Genes
    Associated with Autism Spectrum Disorder.” Institute of Science and Technology
    Austria, 2022. <a href="https://doi.org/10.15479/at:ista:12094">https://doi.org/10.15479/at:ista:12094</a>.
  ieee: C. Dotter, “Transcriptional consequences of mutations in genes associated
    with Autism Spectrum Disorder,” Institute of Science and Technology Austria, 2022.
  ista: Dotter C. 2022. Transcriptional consequences of mutations in genes associated
    with Autism Spectrum Disorder. Institute of Science and Technology Austria.
  mla: Dotter, Christoph. <i>Transcriptional Consequences of Mutations in Genes Associated
    with Autism Spectrum Disorder</i>. Institute of Science and Technology Austria,
    2022, doi:<a href="https://doi.org/10.15479/at:ista:12094">10.15479/at:ista:12094</a>.
  short: C. Dotter, Transcriptional Consequences of Mutations in Genes Associated
    with Autism Spectrum Disorder, Institute of Science and Technology Austria, 2022.
date_created: 2023-01-24T13:09:57Z
date_published: 2022-09-19T00:00:00Z
date_updated: 2023-11-16T13:10:22Z
day: '19'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: GaNo
doi: 10.15479/at:ista:12094
ec_funded: 1
file:
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language:
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month: '09'
oa: 1
oa_version: Published Version
page: '152'
project:
- _id: 254BA948-B435-11E9-9278-68D0E5697425
  grant_number: '401299'
  name: Probing development and reversibility of autism spectrum disorders
- _id: 9B91375C-BA93-11EA-9121-9846C619BF3A
  grant_number: '707964'
  name: Critical windows and reversibility of ASD associated with mutations in chromatin
    remodelers
- _id: 25444568-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '715508'
  name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
    and in vitro Models
- _id: 2690FEAC-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I04205
  name: Identification of converging Molecular Pathways Across Chromatinopathies as
    Targets for Therapy
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
  record:
  - id: '3'
    relation: part_of_dissertation
    status: public
  - id: '11160'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
title: Transcriptional consequences of mutations in genes associated with Autism Spectrum
  Disorder
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2022'
...
---
_id: '8620'
abstract:
- lang: eng
  text: "The development of the human brain occurs through a tightly regulated series
    of dynamic and adaptive processes during prenatal and postnatal life. A disruption
    of this strictly orchestrated series of events can lead to a number of neurodevelopmental
    conditions, including Autism Spectrum Disorders (ASDs). ASDs are a very common,
    etiologically and phenotypically heterogeneous group of disorders sharing the
    core symptoms of social interaction and communication deficits and restrictive
    and repetitive interests and behaviors. They are estimated to affect one in 59
    individuals in the U.S. and, over the last three decades, mutations in more than
    a hundred genetic loci have been convincingly linked to ASD pathogenesis. Yet,
    for the vast majority of these ASD-risk genes their role during brain development
    and precise molecular function still remain elusive.\r\nDe novo loss of function
    mutations in the ubiquitin ligase-encoding gene Cullin 3 (CUL3) lead to ASD. In
    the study described here, we used Cul3 mouse models to evaluate the consequences
    of Cul3 mutations in vivo. Our results show that Cul3 heterozygous knockout mice
    exhibit deficits in motor coordination as well as ASD-relevant social and cognitive
    impairments. Cul3+/-, Cul3+/fl Emx1-Cre and Cul3fl/fl Emx1-Cre mutant brains display
    cortical lamination abnormalities due to defective migration of post-mitotic excitatory
    neurons, as well as reduced numbers of excitatory and inhibitory neurons. In line
    with the observed abnormal cortical organization, Cul3 heterozygous deletion is
    associated with decreased spontaneous excitatory and inhibitory activity in the
    cortex. At the molecular level we show that Cul3 regulates cytoskeletal and adhesion
    protein abundance in the mouse embryonic cortex. Abnormal regulation of cytoskeletal
    proteins in Cul3 mutant neural cells results in atypical organization of the actin
    mesh at the cell leading edge. Of note, heterozygous deletion of Cul3 in adult
    mice does not induce the majority of the behavioral defects observed in constitutive
    Cul3 haploinsufficient animals, pointing to a critical time-window for Cul3 deficiency.\r\nIn
    conclusion, our data indicate that Cul3 plays a critical role in the regulation
    of cytoskeletal proteins and neuronal migration. ASD-associated defects and behavioral
    abnormalities are primarily due to dosage sensitive Cul3 functions at early brain
    developmental stages."
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: I would like to especially thank Armel Nicolas from the Proteomics
  and Christoph Sommer from the Bioimaging Facilities for the data analysis, and to
  thank the team of the Preclinical Facility, especially Sabina Deixler, Angela Schlerka,
  Anita Lepold, Mihalea Mihai and Michael Schun for taking care of the mouse line
  maintenance and their great support.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Jasmin
  full_name: Morandell, Jasmin
  id: 4739D480-F248-11E8-B48F-1D18A9856A87
  last_name: Morandell
citation:
  ama: Morandell J. Illuminating the role of Cul3 in autism spectrum disorder pathogenesis.
    2020. doi:<a href="https://doi.org/10.15479/AT:ISTA:8620">10.15479/AT:ISTA:8620</a>
  apa: Morandell, J. (2020). <i>Illuminating the role of Cul3 in autism spectrum disorder
    pathogenesis</i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:8620">https://doi.org/10.15479/AT:ISTA:8620</a>
  chicago: Morandell, Jasmin. “Illuminating the Role of Cul3 in Autism Spectrum Disorder
    Pathogenesis.” Institute of Science and Technology Austria, 2020. <a href="https://doi.org/10.15479/AT:ISTA:8620">https://doi.org/10.15479/AT:ISTA:8620</a>.
  ieee: J. Morandell, “Illuminating the role of Cul3 in autism spectrum disorder pathogenesis,”
    Institute of Science and Technology Austria, 2020.
  ista: Morandell J. 2020. Illuminating the role of Cul3 in autism spectrum disorder
    pathogenesis. Institute of Science and Technology Austria.
  mla: Morandell, Jasmin. <i>Illuminating the Role of Cul3 in Autism Spectrum Disorder
    Pathogenesis</i>. Institute of Science and Technology Austria, 2020, doi:<a href="https://doi.org/10.15479/AT:ISTA:8620">10.15479/AT:ISTA:8620</a>.
  short: J. Morandell, Illuminating the Role of Cul3 in Autism Spectrum Disorder Pathogenesis,
    Institute of Science and Technology Austria, 2020.
date_created: 2020-10-07T14:53:13Z
date_published: 2020-10-12T00:00:00Z
date_updated: 2024-09-10T12:04:25Z
day: '12'
ddc:
- '610'
degree_awarded: PhD
department:
- _id: GaNo
doi: 10.15479/AT:ISTA:8620
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has_accepted_license: '1'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: '138'
project:
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: W1232-B24
  name: Molecular Drug Targets
- _id: 05A0D778-7A3F-11EA-A408-12923DDC885E
  grant_number: F07807
  name: Neural stem cells in autism and epilepsy
publication_identifier:
  issn:
  - 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
  record:
  - id: '7800'
    relation: part_of_dissertation
    status: public
  - id: '8131'
    relation: part_of_dissertation
    status: public
status: public
supervisor:
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
title: Illuminating the role of Cul3 in autism spectrum disorder pathogenesis
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2020'
...
---
_id: '395'
abstract:
- lang: eng
  text: 'Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping
    with other neurological conditions. Despite the remarkable number of scientific
    breakthroughs of the last 100 years, the treatment of neurodevelopmental disorders
    (e.g. autism spectrum disorder, intellectual disability, epilepsy) remains a great
    challenge. Recent advancements in geno mics, like whole-exome or whole-genome
    sequencing, have enabled scientists to identify numerous mutations underlying
    neurodevelopmental disorders. Given the few hundred risk genes that were discovered,
    the etiological variability and the heterogeneous phenotypic outcomes, the need
    for genotype -along with phenotype- based diagnosis of individual patients becomes
    a requisite. Driven by this rationale, in a previous study our group described
    mutations, identified via whole - exome sequencing, in the gene BCKDK – encoding
    for a key regulator of branched chain amin o acid (BCAA) catabolism - as a cause
    of ASD. Following up on the role of BCAAs, in the study described here we show
    that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter
    localized mainly at the blood brain barrier (BBB), has an essential role in maintaining
    normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial
    cells of the BBB leads to atypical brain amino acid profile, abnormal mRNA translation
    and severe neurolo gical abnormalities. Additionally, deletion of Slc7a5 from
    the neural progenitor cell population leads to microcephaly. Interestingly, we
    demonstrate that BCAA intracerebroventricular administration ameliorates abnormal
    behaviors in adult mutant mice. Furthermore, whole - exome sequencing of patients
    diagnosed with neurological dis o r ders helped us identify several patients with
    autistic traits, microcephaly and motor delay carrying deleterious homozygous
    mutations in the SLC7A5 gene. In conclusion, our data elucidate a neurological
    syndrome defined by SLC7A5 mutations and support an essential role for t he BCAA
    s in human bra in function. Together with r ecent studies (described in chapter
    two) that have successfully made the transition into clinical practice, our findings
    on the role of B CAAs might have a crucial impact on the development of novel
    individualized therapeutic strategies for ASD. '
acknowledged_ssus:
- _id: PreCl
- _id: EM-Fac
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Dora-Clara
  full_name: Tarlungeanu, Dora-Clara
  id: 2ABCE612-F248-11E8-B48F-1D18A9856A87
  last_name: Tarlungeanu
citation:
  ama: Tarlungeanu D-C. The branched chain amino acids in autism spectrum disorders
    . 2018. doi:<a href="https://doi.org/10.15479/AT:ISTA:th_992">10.15479/AT:ISTA:th_992</a>
  apa: Tarlungeanu, D.-C. (2018). <i>The branched chain amino acids in autism spectrum
    disorders </i>. Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th_992">https://doi.org/10.15479/AT:ISTA:th_992</a>
  chicago: Tarlungeanu, Dora-Clara. “The Branched Chain Amino Acids in Autism Spectrum
    Disorders .” Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th_992">https://doi.org/10.15479/AT:ISTA:th_992</a>.
  ieee: D.-C. Tarlungeanu, “The branched chain amino acids in autism spectrum disorders
    ,” Institute of Science and Technology Austria, 2018.
  ista: Tarlungeanu D-C. 2018. The branched chain amino acids in autism spectrum disorders
    . Institute of Science and Technology Austria.
  mla: Tarlungeanu, Dora-Clara. <i>The Branched Chain Amino Acids in Autism Spectrum
    Disorders </i>. Institute of Science and Technology Austria, 2018, doi:<a href="https://doi.org/10.15479/AT:ISTA:th_992">10.15479/AT:ISTA:th_992</a>.
  short: D.-C. Tarlungeanu, The Branched Chain Amino Acids in Autism Spectrum Disorders
    , Institute of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:46:14Z
date_published: 2018-03-01T00:00:00Z
date_updated: 2023-09-07T12:38:59Z
day: '01'
ddc:
- '570'
- '616'
degree_awarded: PhD
department:
- _id: GaNo
doi: 10.15479/AT:ISTA:th_992
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title: 'The branched chain amino acids in autism spectrum disorders '
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