Rebeca Medina

Haga Hospital

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Document Type

Co-Authors

Holger Richly

Institute of Molecular Biology

Jonathan Byrne

King's College Hospital NHS Foundation Trust

Thomas Wilhelm

University College London

Baris Tursun

Universität Hamburg

Johannes Geisinger

Johannes Gutenberg University Mainz

Ena Kolundžić

Humboldt-Universität zu Berlin

Martina Hajdůšková

Charles University

Anna M. Planas

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer

Julián González-Martín

Hospital Clínic de Barcelona

A.S. van der Werf - ’t Lam

Leiden University

Cooperative Institutions

Universitat de Barcelona

Instituto de Salud Carlos III

Institute of Molecular Biology

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer

Universitat Autònoma de Barcelona

Institut d'Investigacions Biomèdiques de Barcelona

Johannes Gutenberg University Mainz

Consejo Superior de Investigaciones Científicas

Centro de Investigación Biomédica en Red

Max Delbrück Center

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Papers

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IFN gamma regulates proliferation and neuronal differentiation by STAT1 in adult SVZ niche

Frontiers in Cellular Neuroscience (2015)

Letícia Pereira Rebeca Medina Miguel Baena Anna M. Planas Esther Pozas

The adult subventricular zone (SVZ) is the main neurogenic niche in normal adult brains of mice and rats. Interferon gamma (IFNγ) has somewhat controversially been associated with SVZ progenitor proliferation and neurogenesis. The in vivo involvement of IFNγ in the physiology of the adult SVZ niche is not fully understood and its intracellular mediators are unknown. Here we show that IFNγ, through activation of its canonical signal transducer and activator of transcription 1 (STAT1) pathway, acts specifically on Nestin+ progenitors by decreasing both progenitor proliferation and the number of cycling cells. In addition, IFNγ increases the number of neuroblasts generated without shifting glial fate determination. The final result is deficient recruitment of newborn neurons to the olfactory bulb (OB), indicating that IFNγ-induced stimulation of neuronal differentiation does not compensate for its antiproliferative effect. We conclude that IFNγ signaling via STAT1 in the SVZ acts dually as an antiproliferative and proneurogenic factor, and thereby regulates neurogenesis in normal adult brains.

Neuroblast

Nestin

Gliogenesis

10.3389/fncel.2015.00270

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Citations (38)

Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans

Genes & Development (2017)

Thomas Wilhelm Jonathan Byrne Rebeca Medina Ena Kolundžić Johannes Geisinger

Autophagy is a ubiquitous catabolic process that causes cellular bulk degradation of cytoplasmic components and is generally associated with positive effects on health and longevity. Inactivation of autophagy has been linked with detrimental effects on cells and organisms. The antagonistic pleiotropy theory postulates that some fitness-promoting genes during youth are harmful during aging. On this basis, we examined genes mediating post-reproductive longevity using an RNAi screen. From this screen, we identified 30 novel regulators of post-reproductive longevity, including pha-4 . Through downstream analysis of pha-4 , we identified that the inactivation of genes governing the early stages of autophagy up until the stage of vesicle nucleation, such as bec-1 , strongly extend both life span and health span. Furthermore, our data demonstrate that the improvements in health and longevity are mediated through the neurons, resulting in reduced neurodegeneration and sarcopenia. We propose that autophagy switches from advantageous to harmful in the context of an age-associated dysfunction.

Pleiotropy

Life span

Model Organism

10.1101/gad.301648.117

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Citations (76)

Andersen-Tawil syndrome: Overlapping clinical features with Noonan syndrome?

European Journal of Medical Genetics (2021)

A.S. van der Werf - ’t Lam Arie van Haeringen T. Rinnen Rebeca Medina Arthur A.M. Wilde

Noonan Syndrome

10.1016/j.ejmg.2021.104382

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Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans

bioRxiv (Cold Spring Harbor Laboratory) (2017)

Thomas Wilhelm Jonathan Byrne Rebeca Medina Ena Kolundžić Johannes Geisinger

Abstract Autophagy is a ubiquitous catabolic process, which causes cellular bulk degradation of cytoplasmic components and thereby regulates cellular homeostasis. Inactivation of autophagy has been linked with detrimental effects to cells and organisms. The antagonistic pleiotropy theory postulates that fitness promoting genes during youth are harmful during aging (Williams 1957). On this basis we examined genes mediating post-reproductive longevity using an RNA interference screen. From this screen we identified 30 novel regulators of post-reproductive longevity including pha-4 . Through downstream analysis of pha-4 we identify that genes governing the early stages of autophagy up until the stage of vesicle nucleation, such as bec-1 , strongly extend both lifespan and healthspan. Further, our data demonstrates that the improvements in health and longevity are mediated through the neurons - resulting in reduced neurodegeneration and sarcopenia. We propose that autophagy switches from advantageous to harmful in the context of an age-associated dysfunction.

Pleiotropy

Catabolism

10.1101/135178

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Citations (1)

The dire side of autophagy in aging: Lessons from C. elegans

Communicative & Integrative Biology (2017)

Rebeca Medina Holger Richly

Autophagy is an essential cellular process that eliminates cellular debris, dysfunctional organelles and misfolded proteins thereby maintaining cellular metabolism and homeostasis. Functional autophagy is generally thought to counteract aging and is crucial for the prolonged lifespan and health of an animal. Whereas this statement is true for young animals, we have recently shown that autophagy becomes dysfunctional in post-reproductive C. elegans contributing to aging and neurodegeneration. Downregulation of autophagy nucleation in post-reproductive nematodes causes a lifespan extension and preservation of neuronal integrity putting the generally accepted view of the role of autophagy in aging into question. Here we discuss specific cellular degradation programs in young and old animals and speculate on molecular mechanisms that might explain this unexpected role of autophagy in aged animals.

10.1080/19420889.2017.1395120

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Physiological, metabolic and haematological responses in white shrimp Litopenaeus vannamei (Boone) juveniles fed diets supplemented with astaxanthin acclimated to low-salinity water

Aquaculture Research (2007)

Maricela Flores Fernando Dı́az Rebeca Medina Ana Denisse Re Alexei F. Licea-Navarro

The effects of dietary astaxanthin supplemented at 0, 40, 80 or 150 mg astaxanthin kg−1 on growth, survival, moult frequency, osmoregulatory capacity (OC) and selected metabolic and haematological variables in Litopenaeus vannamei acclimated to low-salinity water (3 g L−1) were evaluated. Supplemented astaxanthin at 80 mg kg−1 improved growth, survival and moult frequency in shrimp. The lowest OC was also exhibited in shrimp fed with dietary astaxanthin at 80 mg kg−1. Shrimp haemolymph concentrations of glucose, lactate, haemocyanin and total haemocyte count were all significantly enhanced by feeding the diet supplemented with 80 mg astaxanthin kg−1 compared with shrimp fed with the other diets. On the basis of these results, dietary astaxanthin supplementation of 80 mg kg−1 is recommended for juvenile L. vannamei cultured in low-salinity water.

Litopenaeus

Hemolymph

10.1111/j.1365-2109.2007.01720.x

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Citations (67)

Detection of streptomycin and quinolone resistance in Mycobacterium tuberculosis by a low-density DNA array

Tuberculosis (2013)

Raquel Moure Griselda Tudó Rebeca Medina Eva Puy Vicente José María Caldito

Quinolone

10.1016/j.tube.2013.07.001

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Citations (10)

ZRF1 mediates remodeling of E3 ligases at DNA lesion sites during nucleotide excision repair

The Journal of Cell Biology (2016)

Ekaterina Gracheva Shalaka Chitale Thomas Wilhelm Alexander Rapp Jonathan Byrne

Faithful DNA repair is essential to maintain genome integrity. Ultraviolet (UV) irradiation elicits both the recruitment of DNA repair factors and the deposition of histone marks such as monoubiquitylation of histone H2A at lesion sites. Here, we report how a ubiquitin E3 ligase complex specific to DNA repair is remodeled at lesion sites in the global genome nucleotide excision repair (GG-NER) pathway. Monoubiquitylation of histone H2A (H2A-ubiquitin) is catalyzed predominantly by a novel E3 ligase complex consisting of DDB2, DDB1, CUL4B, and RING1B (UV–RING1B complex) that acts early during lesion recognition. The H2A-ubiquitin binding protein ZRF1 mediates remodeling of this E3 ligase complex directly at the DNA lesion site, causing the assembly of the UV–DDB–CUL4A E3 ligase complex (DDB1–DDB2–CUL4A-RBX1). ZRF1 is an essential factor in GG-NER, and its function at damaged chromatin sites is linked to damage recognition factor XPC. Overall, the results shed light on the interplay between epigenetic and DNA repair recognition factors at DNA lesion sites.

DDB1

10.1083/jcb.201506099

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Citations (39)

Determination of the Intracellular, Surface, and Extracellular Localization of Hsp70s under Different Stress Conditions

The FASEB Journal (2012)

Rebeca Medina Manely Rashedan Nikolas Nikolaidis

Members of the Hsp70 family are primarily localized in different subcellular compartments, including the cytosol, endoplasmic reticulum, and mitochondria. Apart from their primary localization, different Hsp70s have also been found in other places within the cell, as well as the cellular membrane and the extracellular milieu. However, it is unknown which stresses are responsible for their re‐localization, membrane translocation, and secretion. To this end we studied the localization of four members of the Hsp70 family under different stresses using sub‐cellular fractionation and confocal microscopy. These experiments revealed that under normal growth conditions all four Hsp70s were present in multiple fractions, as well as in the extracellular medium. In stressed cells, Hsp70 amounts in each fraction were significantly different from the untreated cells. These results suggest that stress causes re‐localization and differential membrane‐anchorage and secretion of the four Hsp70s. Additional experiments using pharmacological manipulation of intracellular trafficking pathways are currently being performed to identify the molecular mechanism used by Hsp70s to achieve their translocation, membrane anchorage, and subsequent secretion. This study is the first step towards elucidating the biological importance of the re‐localization and membrane occurrence of these chaperones. This project was supported by funds from CSUPERB and CSUF to NN.

Cell fractionation

Cell membrane

Cellular compartment

10.1096/fasebj.26.1_supplement.605.2

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Citations (0)

[Protective effect of enprostil on the cells of gastric mucosa damaged by ethanol in the rat. High resolution cytochemical scanning electron microscopy study].

PubMed (1987)

González Angulo A Vilar Rojas C Rebeca Medina Hicks Jj

Source

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