Blanco-Redondo Lab

Our research aims to understand how neurons establish, maintain, and adapt synaptic communication during development and in disease. Using Drosophila melanogaster as a genetically tractable model organism, we combine molecular genetics, cell biology, advanced microscopy, proteomics, and functional analyses to uncover the mechanisms that regulate neuronal connectivity.

​Adhesion GPCR signalling in the nervous system​​

​​​Adhesion G protein-coupled receptors (aGPCRs) are emerging as key regulators of nervous system development and function, yet many remain orphan receptors with poorly understood signalling mechanisms. We investigate the molecular functions of the Drosophila aGPCR family, with a particular focus on the novel receptor Remoulade (CG15744). Our work aims to identify rec​eptor interaction partners, downstream signalling pathways, and the mechanisms by which adhesion GPCRs regulate synapse formation, neuronal communication, and behaviour.

Molecular mechanisms of rare neurodevelopmental disorders​​

​Mutations in genes involved in RNA metabolism can lead to severe neurodevelopmental disorders. We study disease-associated variants of GEMIN5, which cause Neurodevelopmental Disorder with Cerebellar Atrophy and Motor Dysfunction (NEDCAM), using genetically engineered Drosophila models. By investigating how these mutations affect neuronal development and function, we seek to uncover disease mechanisms and identify shared molecular pathways with related motor neuron disorders such as spinal muscular atrophy (SMA).​

​Synaptic communication and circuit plasticity​​​​

Neural circuits must continuously adapt to developmental and physiological changes while maintaining reliable communication. We investigate the molecular mechanisms that regulate synapse assembly, synaptic plasticity, and neuronal connectivity. Our current work particularly focuses on how cell-surface receptors and intercellular signalling pathways shape synaptic architecture and information transfer within defined neural circuits.

From molecules to behaviour​​​

A central goal of our laboratory is to connect molecular mechanisms with nervous system function. We integrate genetics, imaging, electrophysiology, proteomics, and behavioural analyses to understand how alterations at the molecular level influence synaptic function, neural circuit activity, and ultimately animal behaviour.​

• Analysis of the signaling pathway of the adhesion GPCR homolog CG15744/Remoulade in Drosophila (DFG-funded, DFG Individual Grant and associated with the CRC1423)
  
• Circadian tuning of synaptic communication (Tandem project of the Research Training Group-Neurotune, funded through the University of Leipzig)​
  
• Functional analysis of the adhesion GPCR class in Drosophila (in collaboration with Prof. Langenhan)
• Cell biological and molecular analyses on GAIN domain cleavability of adhesion GPCRs​
  
• ​Molecular mechanisms of rare neurodevelopmental disorders ​
  

​

• Alma Radicke - MD candidate
  
• Kaveri Choudhary​ - PhD candidate
• Mariana Herrera​​ Campero - Student helper​
• Paul Goldine​ - MD candidate
  
• Severine Rütze - MD candidate
  
• William Hamlet - PhD Candidate, jointly with the Langenhan lab

Alumni

• Anna Peris Pallàs - Erasmus student, B.Sc. student
  
• Fernando Vieira Contreras - PhD Candidate, jointly with the Langenhan lab
  
• Genevieve Auger​​ - PhD Candidate, jointly with the Langenhan lab
• Irene Ginés - Erasmus student
  
• Javier Pereira - Erasmus student
• Lena Müller - B.Sc./M. Sc. student
• Maurice Schober - B.Sc. student​
• Paul Winter - B.Sc. student
  

​(* equal contribution, ^# correspondence)​

Langenhan T^#, Anderson GR, Araç D, Aust G, Avila-Zozaya M, Bagger SM, Barth P, Berndt S, Blacklow SC, Blanco-Redondo B, Boucard AA, Bridges JP, Brodmerkel LS, Caron KM, Chung YK, Dates AN, Farias V de A, Toro DD, Duman JG, Engel FB, Favara DM, Formstone CJ, Fu C, Bayonas AGDL, Georgiadi A, Gloriam DE, Hall RA, Hamann J, Hildebrand PW, Hsiao CC, Huang BX, Javitch JA, Kim HY, Kittel RJ, Kleinau G, Leduc R, Liebscher I, Lin HH, Linnert J, Ludwig MG, Martinelli DC, Mathiasen S, Matúš D, Melkumyan M, Moreno-Salinas AL, Mulder J, Nash MA, Pal K, Pederick DT, Perry-Hauser NA, Piao X, Ping YQ, Placantonakis DG, Pohl F, Prömel S, Rosenkilde MM, Sabbagh L, Sando RC, Scheerer P, Schöneberg T, Seiradake E, Selcho M, Seufert F, Singh AK, Skiniotis G, Spiess K, Sträter N, Strutt D, Südhof TC, Sun J, Tall GG, Thor D, Tilley DG, Tolias KF, Vallon M, Meir EGV, Vanhollebeke B, Wiggin GR, Wolfrum U, Yan J, Zaidman NA, Zou Y, Scholz N^# (2026). Adhesion G protein-coupled receptors. Pharmacol. Rev., 78, 100116.
DOI: 10.1016/j.pharmr.2026.100116

Contreras FV*, Auger GM*, Müller L, Richter V, Huetteroth W, Seufert F, Hildebrand PW, Scholz N, Thum AS, Ljaschenko D, Blanco-Redondo B^#, Langenhan T^# (2024). The adhesion G-protein-coupled receptor mayo/CG11318 controls midgut development in Drosophila. Cell Rep., 43(1):113640.
DOI: 10.1016/j.celrep.2023.113640​

Scholz N*^#, Dahse AK*, Kemkemer M, Bormann A, Auger GM, Vieira Contreras F, Ernst LF, Staake H, Körner MB, Buhlan M, Meyer-Mölck A, Chung YK, Blanco-Redondo B, Klose F, Jarboui MA, Ljaschenko D, Bigl M, Langenhan T^​# (2023). Molecular sensing of mechano- and ligand-dependent adhesion GPCR dissociation. Nature, 615(7954), 945-953.
DOI: 10.1038/s41586-023-05802-5

Buettner JM*, Sowoidnich L*, Gerstner F, Blanco-Redondo B, Hallermann S, Simon CM (2022). p53-dependent c-Fos expression is a marker but not executor for motor neuron death in spinal muscular atrophy mouse models. Front Cell Neurosci, 16, 1038276.
DOI: 10.3389/fncel.2022.1038276

Korobeynikov VA*, Lyashchenko AK*, Blanco-Redondo B*, Jafar-Nejad P, Shneider NA (2022). Antisense oligonucleotide silencing of FUS expression as a therapeutic approach in amyotrophic lateral sclerosis. Nat Med, 28, 104-116.
DOI: 10.1038/s41591-021-01615-z

Buettner JM*, Sime Longang JKS*, Gerstner F, Apel KS, Blanco-Redondo B, Sowoidnich L, Janzen E, Langenhan T, Wirth B, Simon CM (2021). Central synaptopathy is the most conserved feature of motor circuit pathology across spinal muscular atrophy mouse models. iScience, 24, 103376.
DOI: 10.1016/j.isci.2021.103376

Simon CM, Blanco-Redondo B, Buettner JM, Pagiazitis JG, Fletcher EV, Sime Longang JK, Mentis GZ (2021). Chronic Pharmacological Increase of Neuronal Activity Improves Sensory-Motor Dysfunction in Spinal Muscular Atrophy Mice. J Neurosci, 41, 376-389.
DOI: 10.1523/jneurosci.2142-20.2020

Blanco-Redondo B#, Nuwal N, Kneitz S, Nuwal T, Halder P, Liu Y, Ehmann N, Scholz N, Mayer A, Kleber J, Kahne T, Schmitt D, Sadanandappa MK, Funk N, Albertova V, Helfrich-Forster C, Ramaswami M, Hasan G, Kittel RJ, Langenhan T, Gerber B, Buchner E# (2019). Implications of the Sap47 null mutation for synapsin phosphorylation, longevity, climbing proficiency and behavioural plasticity in adult Drosophila. J Exp Biol, 222, 203505.​
DOI: 10.1242/jeb.203505

Blanco-Redondo B, Langenhan T (2018). Parallel Genomic Engineering of Two Drosophila Genes Using Orthogonal attB/attP Sites. G3 (Bethesda), 8(9), 3109-3118.​
DOI: 10.1534/g3.118.200565

Blanco Redondo B*, Bunz M*, Halder P*​, Sadanandappa MK, Mühlbauer B, Erwin F, Hofbauer A, Rodrigues V, VijayRaghavan K, Ramaswami M, Rieger D, Wegener C, Förster C, Buchner E (2013). Identification and stuctural characterization of interneurons of the Drosophila brain by monoclonal antibodies of the würzburg hybridoma library. Plos One, 8(9):e75420.
DOI: 10.1371/journal.pone.0075420

Sadanandappa MK, Blanco Redondo B, Michels B, Rodrigues V, Gerber B, VijayRaghavan K, Buchner E, Ramaswami M (2013). Synapsin function in Gaba-ergic interneurons is required for short-term olfactory habituation. J Neurosci, 33(42):16576-85.
DOI: 10.1523/jneurosci.3142-13.2013