Lacas-Gervais Sandra
@univ-cotedazur.fr
Life Sciences
Université Côte d'Azur
EDUCATION
Neurosciences PHD
RESEARCH INTERESTS
Cell Biology, Histology, Electron microscopy, Neurosciences, Organelle trafficking, Mitochondrial pathologies
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Sébastien Delhaye, Marielle Jarjat, Asma Boulksibat, Clara Sanchez, Alessandra Tempio, Andrei Turtoi, Mauro Giorgi, Sandra Lacas-Gervais, Gabriele Baj, Carole Rovere,et al.
Elsevier BV
Oleksandr Grytsai, Maeva Dufies, Julie Le Du, Olivia Rastoin, Leticia Christina Pires Gonçalves, Lou Mateo, Sandra Lacas-Gervais, Yihai Cao, Luc Demange, Gilles Pagès,et al.
American Chemical Society (ACS)
Mélody Subra, Manuela Dezi, Joëlle Bigay, Sandra Lacas-Gervais, Aurélie Di Cicco, Ana Rita Dias Araújo, Sophie Abélanet, Lucile Fleuriot, Delphine Debayle, Romain Gautier,et al.
Elsevier BV
Emmanuelle C Genin, Sylvie Bannwarth, Baptiste Ropert, Françoise Lespinasse, Alessandra Mauri-Crouzet, Gaelle Augé, Konstantina Fragaki, Charlotte Cochaud, Erminia Donnarumma, Sandra Lacas-Gervais,et al.
Oxford University Press (OUP)
Abstract CHCHD10 is an amyotrophic lateral sclerosis/frontotemporal dementia gene that encodes a mitochondrial protein whose precise function is unclear. Here we show that Coiled-Coil-Helix-Coiled-Coil-Helix Domain Containing protein 10 interacts with the Stomatin-Like Protein 2 and participates in the stability of the prohibitin complex in the inner mitochondrial membrane. By using patient fibroblasts and mouse models expressing the same CHCHD10 variant (p.Ser59Leu), we show that Stomatin-Like Protein 2 forms aggregates with prohibitins, found in vivo in the hippocampus and as aggresome-like inclusions in spinal motor neurons of Chchd10S59L/+ mice. Affected cells and tissues display instability of the prohibitin complex, which participates at least in part in the activation of the OMA1 cascade with OPA1 processing leading to mitochondrial fragmentation, abnormal mitochondrial cristae morphogenesis and neuronal death found in spinal cord and the hippocampus of Chchd10S59L/+ animals. Destabilization of the prohibitin complex leads to the instability of the mitochondrial contact site and cristae organizing the system complex, probably by the disruption of OPA1–mitofilin interaction. Thus, Stomatin-Like Protein 2/prohibitin aggregates and destabilization of the prohibitin complex are critical in the sequence of events leading to motor neuron death in CHCHD10S59L-related disease.
Charlotte Corporeau, Sébastien Petton, Romain Vilaça, Lizenn Delisle, Claudie Quéré, Valérian Le Roy, Christine Dubreuil, Sandra Lacas-Gervais, Yann Guitton, Sébastien Artigaud,et al.
Elsevier BV
Dawei Liu, Félix Peyre, Yahir Alberto Loissell-Baltazar, Delphine Courilleau, Sandra Lacas-Gervais, Valérie Nicolas, Eric Jacquet, Svetlana Dokudovskaya, Frédéric Taran, Jean-Christophe Cintrat,et al.
MDPI AG
Improvement of anticancer treatments is associated with increased survival of cancer patients at risk of cardiac disease. Therefore, there is an urgent need for new therapeutic molecules capable of preventing acute and long-term cardiotoxicity. Here, using commercial and home-made chemolibraries, we performed a robust phenotypic high-throughput screening in rat cardiomyoblast cell line H9c2, searching for small molecules capable of inhibiting cell death. A screen of 1600 compounds identified six molecules effective in preventing necrosis and apoptosis induced by H2O2 and camptothecin in H9c2 cells and in rat neonatal ventricular myocytes. In cells treated with these molecules, we systematically evaluated the expression of BCL-2 family members, autophagy progression, mitochondrial network structure, regulation of mitochondrial fusion/fission, reactive oxygen species, and ATP production. We found that these compounds affect autophagy induction to prevent cardiac cell death and can be promising cardioprotective drugs during chemotherapy.
M. Christiane Brahimi-Horn, Sandra Lacas-Gervais, Ricardo Adaixo, Karine Ilc, Matthieu Rouleau, Annick Notte, Marc Dieu, Carine Michiels, Thibault Voeltzel, Véronique Maguer-Satta,et al.
American Society for Microbiology
M. Christiane Brahimi-Horn, Sandra Lacas-Gervais, Ricardo Adaixo, Karine Ilc, Matthieu Rouleau, Annick Notte, Marc Dieu, Carine Michiels, Thibault Voeltzel, Véronique Maguer-Satta,et al.
American Society for Microbiology
Aurélie Schwing, Didier F. Pisani, Christelle Pomares, Alissa Majoor, Sandra Lacas-Gervais, Jennifer Jager, Emmanuel Lemichez, Pierre Marty, Laurent Boyer, and Grégory Michel
Springer Science and Business Media LLC
AbstractLeishmania infantum is the causative agent of visceral leishmaniasis transmitted by the bite of female sand flies. According to the WHO, the estimated annual incidence of leishmaniasis is one million new cases, resulting in 30,000 deaths per year. The recommended drugs for treating leishmaniasis include Amphotericin B. But over the course of the years, several cases of relapses have been documented. These relapses cast doubt on the efficiency of actual treatments and raise the question of potential persistence sites. Indeed, Leishmania has the ability to persist in humans for long periods of time and even after successful treatment. Several potential persistence sites have already been identified and named as safe targets. As adipose tissue has been proposed as a sanctuary of persistence for several pathogens, we investigated whether Leishmania infantum could be found in this tissue. We demonstrated both in cell cultures and in vivo that Leishmania infantum was able to infect adipocytes. Altogether our results suggest adipocytes as a ‘safe target’ for Leishmania infantum parasites.
Audrey Valverde, Julie Dunys, Thomas Lorivel, Delphine Debayle, Anne-Sophie Gay, Sandra Lacas-Gervais, Bernard. P. Roques, Mounia Chami, and Frédéric Checler
Springer Science and Business Media LLC
AbstractOne of the main components of senile plaques in Alzheimer’s disease (AD)-affected brain is the Aβ peptide species harboring a pyroglutamate at position three pE3-Aβ. Several studies indicated that pE3-Aβ is toxic, prone to aggregation and serves as a seed of Aβ aggregation. The cyclisation of the glutamate residue is produced by glutaminyl cyclase, the pharmacological and genetic reductions of which significantly alleviate AD-related anatomical lesions and cognitive defects in mice models. The cyclisation of the glutamate in position 3 requires prior removal of the Aβ N-terminal aspartyl residue to allow subsequent biotransformation. The enzyme responsible for this rate-limiting catalytic step and its relevance as a putative trigger of AD pathology remained yet to be established. Here, we identify aminopeptidase A as the main exopeptidase involved in the N-terminal truncation of Aβ and document its key contribution to AD-related anatomical and behavioral defects. First, we show by mass spectrometry that human recombinant aminopeptidase A (APA) truncates synthetic Aβ1-40 to yield Aβ2-40. We demonstrate that the pharmacological blockade of APA with its selective inhibitor RB150 restores the density of mature spines and significantly reduced filopodia-like processes in hippocampal organotypic slices cultures virally transduced with the Swedish mutated Aβ-precursor protein (βAPP). Pharmacological reduction of APA activity and lowering of its expression by shRNA affect pE3-42Aβ- and Aβ1-42-positive plaques and expressions in 3xTg-AD mice brains. Further, we show that both APA inhibitors and shRNA partly alleviate learning and memory deficits observed in 3xTg-AD mice. Importantly, we demonstrate that, concomitantly to the occurrence of pE3-42Aβ-positive plaques, APA activity is augmented at early Braak stages in sporadic AD brains. Overall, our data indicate that APA is a key enzyme involved in Aβ N-terminal truncation and suggest the potential benefit of targeting this proteolytic activity to interfere with AD pathology.
Stéphanie Torrino, Victor Tiroille, Bastien Dolfi, Maeva Dufies, Charlotte Hinault, Laurent Bonesso, Sonia Dagnino, Jennifer Uhler, Marie Irondelle, Anne-sophie Gay,et al.
eLife Sciences Publications, Ltd
To adapt in an ever-changing environment, cells must integrate physical and chemical signals and translate them into biological meaningful information through complex signaling pathways. By combining lipidomic and proteomic approaches with functional analysis, we have shown that ubiquitin domain-containing protein 1 (UBTD1) plays a crucial role in both the epidermal growth factor receptor (EGFR) self-phosphorylation and its lysosomal degradation. On the one hand, by modulating the cellular level of ceramides through N-acylsphingosine amidohydrolase 1 (ASAH1) ubiquitination, UBTD1 controls the ligand-independent phosphorylation of EGFR. On the other hand, UBTD1, via the ubiquitination of Sequestosome 1 (SQSTM1/p62) by RNF26 and endolysosome positioning, participates in the lysosomal degradation of EGFR. The coordination of these two ubiquitin-dependent processes contributes to the control of the duration of the EGFR signal. Moreover, we showed that UBTD1 depletion exacerbates EGFR signaling and induces cell proliferation emphasizing a hitherto unknown function of UBTD1 in EGFR-driven human cell proliferation.
Wejdane El Manaa, Eric Duplan, Thomas Goiran, Inger Lauritzen, Loan Vaillant Beuchot, Sandra Lacas-Gervais, Vanessa Alexandra Morais, Han You, Ling Qi, Mario Salazar,et al.
Informa UK Limited
ABSTRACT Parkinson disease (PD)-affected brains show consistent endoplasmic reticulum (ER) stress and mitophagic dysfunctions. The mechanisms underlying these perturbations and how they are directly linked remain a matter of questions. XBP1 is a transcription factor activated upon ER stress after unconventional splicing by the nuclease ERN1/IREα thereby yielding XBP1s, whereas PINK1 is a kinase considered as the sensor of mitochondrial physiology and a master gatekeeper of mitophagy process. We showed that XBP1s transactivates PINK1 in human cells, primary cultured neurons and mice brain, and triggered a pro-mitophagic phenotype that was fully dependent of endogenous PINK1. We also unraveled a PINK1-dependent phosphorylation of XBP1s that conditioned its nuclear localization and thereby, governed its transcriptional activity. PINK1-induced XBP1s phosphorylation occurred at residues reminiscent of, and correlated to, those phosphorylated in substantia nigra of sporadic PD-affected brains. Overall, our study delineated a functional loop between XBP1s and PINK1 governing mitophagy that was disrupted in PD condition. Abbreviations: 6OHDA: 6-hydroxydopamine; baf: bafilomycin A1; BECN1: beclin 1; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CASP3: caspase 3; CCCP: carbonyl cyanide chlorophenylhydrazone; COX8A: cytochrome c oxidase subunit 8A; DDIT3/CHOP: DNA damage inducible transcript 3; EGFP: enhanced green fluorescent protein; ER: endoplasmic reticulum; ERN1/IRE1α: endoplasmic reticulum to nucleus signaling 1; FACS: fluorescence-activated cell sorting; HSPD1/HSP60: heat shock protein family D (Hsp60) member 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MFN2: mitofusin 2; OPTN: optineurin; PD: Parkinson disease; PINK1: PTEN-induced kinase 1; PCR: polymerase chain reaction:; PRKN: parkin RBR E3 ubiquitin protein ligase; XBP1s [p-S61A]: XBP1s phosphorylated at serine 61; XBP1s [p-T48A]: XBP1s phosphorylated at threonine 48; shRNA: short hairpin RNA, SQSTM1/p62: sequestosome 1; TIMM23: translocase of inner mitochondrial membrane 23; TM: tunicamycin; TMRM: tetramethyl rhodamine methylester; TOMM20: translocase of outer mitochondrial membrane 20; Toy: toyocamycin; TP: thapsigargin; UB: ubiquitin; UB (S65): ubiquitin phosphorylated at serine 65; UPR: unfolded protein response, XBP1: X-box binding protein 1; XBP1s: spliced X-box binding protein 1
Mariagrazia Partisani, Carole L. Baron, Rania Ghossoub, Racha Fayad, Sophie Pagnotta, Sophie Abélanet, Eric Macia, Frédéric Brau, Sandra Lacas-Gervais, Alexandre Benmerah,et al.
The Company of Biologists
ABSTRACT Ciliogenesis is a coordinated process initiated by the recruitment and fusion of pre-ciliary vesicles at the distal appendages of the mother centriole through mechanisms that remain unclear. Here, we report that EFA6A (also known as PSD), an exchange factor for the small G protein Arf6, is involved in early stage of ciliogenesis by promoting the fusion of distal appendage vesicles forming the ciliary vesicle. EFA6A is present in the vicinity of the mother centriole before primary cilium assembly and prior to the arrival of Arl13B-containing vesicles. During ciliogenesis, EFA6A initially accumulates at the mother centriole and later colocalizes with Arl13B along the ciliary membrane. EFA6A depletion leads to the inhibition of ciliogenesis, the absence of centrosomal Rab8-positive structures and the accumulation of Arl13B-positive vesicles around the distal appendages. Our results uncover a novel fusion machinery, comprising EFA6A, Arf6 and Arl13B, that controls the coordinated fusion of ciliary vesicles docked at the distal appendages of the mother centriole.
Loan Vaillant-Beuchot, Arnaud Mary, Raphaëlle Pardossi-Piquard, Alexandre Bourgeois, Inger Lauritzen, Fanny Eysert, Paula Fernanda Kinoshita, Julie Cazareth, Céline Badot, Konstantina Fragaki,et al.
Acta Neuropathologica Springer Science and Business Media LLC
AbstractSeveral lines of recent evidence indicate that the amyloid precursor protein-derived C-terminal fragments (APP-CTFs) could correspond to an etiological trigger of Alzheimer’s disease (AD) pathology. Altered mitochondrial homeostasis is considered an early event in AD development. However, the specific contribution of APP-CTFs to mitochondrial structure, function, and mitophagy defects remains to be established. Here, we demonstrate in neuroblastoma SH-SY5Y cells expressing either APP Swedish mutations, or the β-secretase-derived APP-CTF fragment (C99) combined with β- and γ-secretase inhibition, that APP-CTFs accumulation independently of Aβ triggers excessive mitochondrial morphology alteration (i.e., size alteration and cristae disorganization) associated with enhanced mitochondrial reactive oxygen species production. APP-CTFs accumulation also elicit basal mitophagy failure illustrated by enhanced conversion of LC3, accumulation of LC3-I and/or LC3-II, non-degradation of SQSTM1/p62, inconsistent Parkin and PINK1 recruitment to mitochondria, enhanced levels of membrane and matrix mitochondrial proteins, and deficient fusion of mitochondria with lysosomes. We confirm the contribution of APP-CTFs accumulation to morphological mitochondria alteration and impaired basal mitophagy in vivo in young 3xTgAD transgenic mice treated with γ-secretase inhibitor as well as in adeno-associated-virus-C99 injected mice. Comparison of aged 2xTgAD and 3xTgAD mice indicates that, besides APP-CTFs, an additional contribution of Aβ to late-stage mitophagy activation occurs. Importantly, we report on mitochondrial accumulation of APP-CTFs in human post-mortem sporadic AD brains correlating with mitophagy failure molecular signature. Since defective mitochondria homeostasis plays a pivotal role in AD pathogenesis, targeting mitochondrial dysfunctions and/or mitophagy by counteracting early APP-CTFs accumulation may represent relevant therapeutic interventions in AD.
Monique Meyenberg Cunha-de Padua, Lucilla Fabbri, Maeva Dufies, Sandra Lacas-Gervais, Julie Contenti, Charles Voyton, Sofia Fazio, Marie Irondelle, Baharia Mograbi, Matthieu Rouleau,et al.
MDPI AG
Metabolic flexibility is the ability of a cell to adapt its metabolism to changes in its surrounding environment. Such adaptability, combined with apoptosis resistance provides cancer cells with a survival advantage. Mitochondrial voltage-dependent anion channel 1 (VDAC1) has been defined as a metabolic checkpoint at the crossroad of these two processes. Here, we show that the hypoxia-induced cleaved form of VDAC1 (VDAC1-ΔC) is implicated in both the up-regulation of glycolysis and the mitochondrial respiration. We demonstrate that VDAC1-ΔC, due to the loss of the putative phosphorylation site at serine 215, concomitantly with the loss of interaction with tubulin and microtubules, reprograms the cell to utilize more metabolites, favoring cell growth in hypoxic microenvironment. We further found that VDAC1-ΔC represses ciliogenesis and thus participates in ciliopathy, a group of genetic disorders involving dysfunctional primary cilium. Cancer, although not representing a ciliopathy, is tightly linked to cilia. Moreover, we highlight, for the first time, a direct relationship between the cilium and cancer cell metabolism. Our study provides the first new comprehensive molecular-level model centered on VDAC1-ΔC integrating metabolic flexibility, ciliogenesis, and enhanced survival in a hypoxic microenvironment.
Alix Dubois, Nathan Furstoss, Anne Calleja, Marwa Zerhouni, Thomas Cluzeau, Coline Savy, Sandrine Marchetti, Mohamed Amine Hamouda, Sonia Boulakirba, François Orange,et al.
Springer Science and Business Media LLC
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Laurent Grosse, Nicole Wagner, Alexander Emelyanov, Clement Molina, Sandra Lacas-Gervais, Kay-Dietrich Wagner, and Dmitry V. Bulavin
Elsevier BV
Clémence M. Canivet, Stéphanie Bonnafous, Déborah Rousseau, Pierre S. Leclere, Sandra Lacas-Gervais, Stéphanie Patouraux, Arnaud Sans, Carmelo Luci, Béatrice Bailly-Maitre, Antonio Iannelli,et al.
Elsevier BV
Karine Dumas, Chaima Ayachi, Jerome Gilleron, Sandra Lacas‐Gervais, Faustine Pastor, François B. Favier, Pascal Peraldi, Nathalie Vaillant, Laurent Yvan‐Charvet, Stéphanie Bonnafous,et al.
Wiley
Nonalcoholic fatty liver disease is a chronic liver disease which is associated with obesity and insulin resistance. We investigated the implication of REDD1 (Regulated in development and DNA damage response‐1), a stress‐induced protein in the development of hepatic steatosis. REDD1 expression was increased in the liver of obese mice and morbidly obese patients, and its expression correlated with hepatic steatosis and insulin resistance in obese patients. REDD1 deficiency protected mice from the development of hepatic steatosis induced by high‐fat diet (HFD) without affecting body weight gain and glucose intolerance. This protection was associated with a decrease in the expression of lipogenic genes, SREBP1c, FASN, and SCD‐1 in liver of HFD‐fed REDD1‐KO mice. Healthy mitochondria are crucial for the adequate control of lipid metabolism and failure to remove damaged mitochondria is correlated with liver steatosis. Expression of markers of autophagy and mitophagy, Beclin, LC3‐II, Parkin, BNIP3L, was enhanced in liver of HFD‐fed REDD1‐KO mice. The number of mitochondria showing colocalization between LAMP2 and AIF was increased in liver of HFD‐fed REDD1‐KO mice. Moreover, mitochondria in liver of REDD1‐KO mice were smaller than in WT. These results are correlated with an increase in PGC‐1α and CPT‐1 expression, involved in fatty acid oxidation. In conclusion, loss of REDD1 protects mice from the development of hepatic steatosis.
Lucilla Fabbri, Maeva Dufies, Sandra Lacas-Gervais, Betty Gardie, Sophie Gad-Lapiteau, Julien Parola, Nicolas Nottet, Monique Meyenberg Cunha de Padua, Julie Contenti, Delphine Borchiellini,et al.
Ivyspring International Publisher
Rationale: Renal cell carcinoma (RCC) accounts for about 2% of all adult cancers, and clear cell RCC (ccRCC) is the most common RCC histologic subtype. A hallmark of ccRCC is the loss of the primary cilium, a cellular antenna that senses a wide variety of signals. Loss of this key organelle in ccRCC is associated with the loss of the von Hippel-Lindau protein (VHL). However, not all mechanisms of ciliopathy have been clearly elucidated. Methods: By using RCC4 renal cancer cells and patient samples, we examined the regulation of ciliogenesis via the presence or absence of the hypoxic form of the voltage-dependent anion channel (VDAC1-ΔC) and its impact on tumor aggressiveness. Three independent cohorts were analyzed. Cohort A was from PREDIR and included 12 patients with hereditary pVHL mutations and 22 sporadic patients presenting tumors with wild-type pVHL or mutated pVHL; Cohort B included tissue samples from 43 patients with non-metastatic ccRCC who had undergone surgery; and Cohort C was composed of 375 non-metastatic ccRCC tumor samples from The Cancer Genome Atlas (TCGA) and was used for validation. The presence of VDAC1-ΔC and legumain was determined by immunoblot. Transcriptional regulation of IFT20/GLI1 expression was evaluated by qPCR. Ciliogenesis was detected using both mouse anti-acetylated α-tubulin and rabbit polyclonal ARL13B antibodies for immunofluorescence. Results: Our study defines, for the first time, a group of ccRCC patients in which the hypoxia-cleaved form of VDAC1 (VDAC1-ΔC) induces resorption of the primary cilium in a Hypoxia-Inducible Factor-1 (HIF-1)-dependent manner. An additional novel group, in which the primary cilium is re-expressed or maintained, lacked VDAC1-ΔC yet maintained glycolysis, a signature of epithelial-mesenchymal transition (EMT) and more aggressive tumor progression, but was independent to VHL. Moreover, these patients were less sensitive to sunitinib, the first-line treatment for ccRCC, but were potentially suitable for immunotherapy, as indicated by the immunophenoscore and the presence of PDL1 expression. Conclusion: This study provides a new way to classify ccRCC patients and proposes potential therapeutic targets linked to metabolism and immunotherapy.
Eric Macia, Mariagrazia Partisani, Hong Wang, Sandra Lacas-Gervais, Christophe Le Clainche, Frederic Luton, and Michel Franco
Springer Science and Business Media LLC
AbstractThe Arf6-specific exchange factor EFA6 is involved in the endocytic/recycling pathway for different cargos. In addition EFA6 acts as a powerful actin cytoskeleton organizer, a function required for its role in the establishment of the epithelial cell polarity and in neuronal morphogenesis. We previously showed that the C-terminus of EFA6 (EFA6-Ct) is the main domain which contributes to actin reorganization. Here, byin vitroandin vivoexperiments, we sought to decipher, at the molecular level, how EFA6 controls the dynamic and structuring of actin filaments. We showed that EFA6-Ct interferes with actin polymerization by interacting with and capping actin filament barbed ends. Further, in the presence of actin mono-filaments, the addition of EFA6-Ct triggered the formation of actin bundles. In cells, when the EFA6-Ct was directed to the plasma membrane, as is the case for the full-length protein, its expression induced the formation of membrane protrusions enriched in actin cables. Collectively our data explain, at least in part, how EFA6 plays an essential role in actin organization by interacting with and bundling F-actin.
Malika Arhatte, Gihan S. Gunaratne, Charbel El Boustany, Ivana Y. Kuo, Céline Moro, Fabrice Duprat, Magali Plaisant, Hélène Duval, Dahui Li, Nicolas Picard,et al.
Springer Science and Business Media LLC
Alix Dubois, Nathan Furstoss, Anne Calleja, Marwa Zerhouni, Thomas Cluzeau, Coline Savy, Sandrine Marchetti, Mohamed Amine Hamouda, Sonia Boulakirba, François Orange,et al.
Springer Science and Business Media LLC
Emmanuelle C. Genin, Blandine Madji Hounoum, Sylvie Bannwarth, Konstantina Fragaki, Sandra Lacas-Gervais, Alessandra Mauri-Crouzet, Françoise Lespinasse, Julien Neveu, Baptiste Ropert, Gaelle Augé,et al.
Springer Science and Business Media LLC
Allon Weiner, François Orange, Sandra Lacas‐Gervais, Katya Rechav, Vikram Ghugtyal, Martine Bassilana, and Robert A. Arkowitz
Hindawi Limited
Candida albicans is an opportunistic fungal pathogen that colonises the skin as well as genital and intestinal mucosa of most healthy individuals. The ability of C. albicans to switch between different morphological states, for example, from an ellipsoid yeast form to a highly polarised, hyphal form, contributes to its success as a pathogen. In highly polarised tip‐growing cells such as neurons, pollen tubes, and filamentous fungi, delivery of membrane and cargo to the filament apex is achieved by long‐range delivery of secretory vesicles tethered to motors moving along cytoskeletal cables that extend towards the growing tip. To investigate whether such a mechanism is also critical for C. albicans filamentous growth, we studied the dynamics and organisation of the C. albicans secretory pathway using live cell imaging and three‐dimensional electron microscopy. We demonstrate that the secretory pathway is organised in distinct domains, including endoplasmic reticulum membrane sheets that extend along the length of the hyphal filament, a sub‐apical zone exhibiting distinct membrane structures and dynamics and a Spitzenkörper comprised of uniformly sized secretory vesicles. Our results indicate that the organisation of the secretory pathway in C. albicans likely facilitates short‐range “on‐site” secretory vesicle delivery, in contrast to filamentous fungi and many highly polarised cells.