Biology subjects

Oliveira, L.

Publications and source records attributed to Oliveira, L..

At least 19 recordsLinked to original sources

bioRxiv2026

An atlas of eukaryotic centromere architecture reveals recurrent evolutionary dynamics

Centromeres evolved at the root of eukaryotes to segregate chromosomes during cell division. Despite their ancient origin, centromeric DNA sequences evolve rapidly and adopt diverse architectures, including point centromeres, satellite arrays, transposon clusters, and holocentrics. To analyse centromere evolution at a broad scale, we characterised architectures across 325 diverse Darwin Tree of Life genome assemblies. Centromere architecture is evolutionarily labile, and similar configurations arise independently across divergent lineages. In plants and animals, we modelled centromere evolution as a recurrent cycle, in which satellite- and transposon-based architectures interconvert, with independent origins of holocentricity. We curated >23 million satellite repeats comprising 263 families from 165 species. Despite sequence divergence between satellite families, higher order repeats are prevalent, indicating constraint on repeat architecture rather than primary sequence. Satellite arrays are heavily invaded by diverse transposon families, consistent with convergent adaptation to the centromeric niche. In 89 species, transposons themselves constitute the primary centromere structure. We observed centrophilic transposons forming tandem arrays, suggesting mechanisms for satellite regeneration. Our sample includes five independent origins of holocentricity in plants and animals, which vary in association with periodic satellite arrays. We propose that genetic instability, centrophilic transposition, and transmission distortion promote recurrent centromere architectural interconversions during evolution.

genomics↗

bioRxiv2026

TFE3 fusions drive expression of CD44 and SPP1 in Translocation Renal Cell Carcinoma

Xp11.2 translocation RCC [Xp11.2 tRCC]) is an underdiagnosed and aggressive subtype of RCC with few specific or targeted therapies. The transmembrane glycoprotein CD44 is an emerging target in many advanced malignancies, and with its ligand OPN (SPP1), is a crucial driver of cancer progression, stemness, metastasis, and immune suppression. Here we show that common TFE3-fusions [ including SFPQ-TFE3, PRCC-TFE3, ASPSCR1-TFE3, and NONO-TFE3] are associated with upregulated expression of CD44 and SPP1, as observed in multiple human and murine bulk transcriptomic studies and a murine tRCC snRNA-Seq dataset. CD44 and/or SPP1 protein expression were also upregulated in murine models of transgenic tRCC kidneys and urine specimens, patient-derived cell lines and human tRCC cases, by immunoblotting and/or IHC. Transient deletion of CD44 was associated with profound and specific suppression of tRCC cell line growth, with decreased mTOR signaling. These data suggest that CD44 and/or SPP1 may potentially drive tumorigenesis in tRCC.

cancer biology↗

bioRxiv2026

THE STRUCTURES OF MATURE AND IMMATURE ST. LOUIS ENCEPHALITIS VIRUS REVEAL CONSERVED HISTIDINE RESIDUES AFFECTING VIRUS FITNESS

Orthoflaviviruses undergo significant structural changes through maturation and infection, yet the molecular mechanisms remain incompletely understood. Using St. Louis encephalitis virus (SLEV) as a model, a reemerging mosquito-borne orthoflavivirus endemic in the Americas, we elucidated the structures of immature and mature SLEV particles at resolutions of 4.4 [A] and 3.3 [A], respectively, using cryo-EM. SLEV is characterized by glycosylated E and prM proteins, the presence of lipid pockets, and is stabilized by an intricate network of inter- and intra-protein interactions between E and (pr)M across maturation stages. Several interactions were mediated by histidines that play different roles depending on SLEV maturation and pH. Non-lethal single mutations of H285R and H443R in E protein affect SLEV replication in mammalian and mosquito cell lines, and delay death in mouse models of infection. These histidine residues are conserved across orthoflaviviruses, illustrating the complexity of orthoflavivirus particles and indicating a possible strategy for attenuation.

microbiology↗

bioRxiv2025

CD5L insufficiency exacerbates skeletal joint damage in rheumatoid arthritis

CD5L is an immunoregulatory protein induced during inflammation and makes a life-saving contribution in infection and sepsis. Here, we explored the overall impact of CD5L in rheumatoid arthritis (RA). Using experimental RA models, we demonstrated an early surge of CD5L expression in wild-type mice, as well as a higher incidence and increased severity of arthritis in CD5L-deficient mice. In the blood, CD5L-deficient mice exhibited enhanced inflammation, a higher proportion of CD11b mononuclear cells, and elevated levels of IL-1{beta}, IL-17, and IFN-{psi}, particularly at the pre-clinical stage of arthritis. In human RA, mononuclear cells conditioned with CD5L, as well as endogenous CD5L production, were associated with reduced CD11b expression, increased IL-10 and PD-L1 production, and an enrichment of non-classical CD16+ monocytes. Analysis of the CD5L-dependent transcriptome in CD14 cells from RA patients revealed the acquisition of an efferocytosis profile, with upregulation of C1Q subunits, GAS6, AXL, and ALOX15B. It also showed signs of insufficient cargo processing, which dampens the resolution of inflammation, permits the expansion of IFN-primed non-classical monocytes, and correlates strongly with joint damage accrual. Despite markedly low CD5L levels in the synovium, RA synovial tissue was enriched with non-classical monocytes carrying the GAS6-AXL signature, which fosters osteoclast progenitors. In conclusion, this study demonstrates that the anti-inflammatory and inflammation-resolving properties of CD5L in experimental and human RA are mediated through the induction of efferocytosis-related and IFN-primed monocyte programs. This harbors a potential risk of uncontrolled invasion of non-classical monocytes into the synovial tissue, leading to joint structural damage. The complex role of CD5L in inflammation and disease outcomes requires careful consideration of the disease phase and experimental context.

immunology↗

bioRxiv2025

Chart Builder: An Interactive Tool for User Driven Data Visualization in the Electron Microscopy Data Bank

The cryogenic sample-electron microscopy (cryoEM) field has generated significant amounts of 3D Electron Microscopy (3DEM) volumetric data and associated metadata, now comprehensively archived in the Electron Microscopy Data Bank (EMDB - www.emdatabank.org) and the Electron Microscopy Public Image Archive (EMPIAR - www.empiar.org). Harnessing the full potential of these resources requires robust, flexible, and publicly accessible tools for data exploration, analysis and retrieval. Here, we present Chart Builder, an interactive web-based platform that enables researchers to create customizable, publication-quality visualizations directly from archival metadata, validation assessments, and cross-reference annotations. Chart Builder integrates the same query-driven and flexible Solr search system as EMDB search, into a user interface with tools to assist users to filter, group, and compare data without programming expertise. It supports multiple chart types (including line, bar, area, scatter (2D and 3D), histogram, bubble, pie, geographic and Venn diagrams) with customizable axes, data series, and statistical operators. Users can apply global filters, define temporal, categorical, or custom query-based axes, and explore multi-dimensional relationships interactively. Chart data-points are linked to their underlying datasets, such that visualisation interaction opens entry-level or archive-level search results for inspection and datasets from charts may be exported in several ways. Findability, accessibility, interoperability and reusability of data are facilitated by these direct access and export mechanisms, including HTML embedding, persistent URL sharing and chart/data download options. By combining interactivity and ease of use with up-to-date access to the EMDB and EMPIAR archive metadata, both computational and experimental communities may explore and visualize current metadata and export to formats for further analysis or as publication-ready figures. Chart Builder promotes community-driven data analysis and empowers users to evaluate trends in the biological 3DEM field. Chart Builder is freely accessible and fully integrated into the EMDB website at https://www.ebi.ac.uk/emdb/statistics/builder/.

biophysics↗

bioRxiv2025

Engineering surface electrostatics affords control over morphological preference, synergy, and activity in polymer degrading enzymes

The biocatalytic recycling of plastics, such as polyethylene terephthalate (PET), promises a sustainable alternative to our present open-loop cycles. Engineering of PET-hydrolases for this purpose has focused on improving activity near the glass-transition temperature of the polymer by increasing their thermostability, neglecting other features of the protein-polymer system that affect enzymatic activity. Here, we isolate the effect of electrostatics on the activity of a thermophilic PETase by rationally redesigning its surface charge, while preserving its thermodynamic properties. The enzyme variant, SfInv, shows orders of magnitude improvements in binding affinity and in activity towards untreated plastic films, with inverted morphological preference. When combined, the wildtype enzyme and SfInv act synergistically, revealing an entirely new mechanism for cooperative activities driven by complimentary electrostatic interactions at the PET surface. These findings highlight unexplored avenues in improving PETase function through the control of morphological preference or introduction of protein cooperativity by exploiting protein electrostatics.

biochemistry↗

bioRxiv2024

AIP56, an AB toxin secreted by Photobacterium damselae subsp. piscicida, has tropism for myeloid cells

The AB-type toxin AIP56 is a key virulence factor of Photobacterium damselae subsp. piscicida (Phdp), inducing apoptosis in fish immune cells. The discovery of AIP56-like and AIP56-related toxins in diverse organisms, including human-associated Vibrio strains, highlights the evolutionary conservation of this toxin family, suggesting that AIP56 and its homologs may share conserved receptors across species. These toxins have potential for biotechnological applications, such as therapeutic protein delivery and immune modulation. Herein, the cell specificity of AIP56 for immune cells in sea bass, mice, and humans was characterized. Whether AIP56 interacts directly or indirectly with sea bass neutrophils was never investigated and it was shown that only a small population of sea bass neutrophils internalized AIP56, indicating that most of the neutrophilic destruction during Phdp infection and/or AIP56 intoxication does not result from the direct toxicity of the toxin. Moreover, the cellular tropism of AIP56 for myeloid cells was observed in the three species, including its preference for macrophages. Further, mouse and human M0 and M2-like macrophages internalized more toxin than M1-like macrophages. Despite the limited interaction of lymphoid cells with AIP56, mouse B1-cells were able to internalize the toxin, possibly due to its myeloid features. These findings are relevant for both pathogenicity and biomedical contexts.

immunology↗

bioRxiv2024

SYSTEMIC FRATAXIN DEFICIENCY CAUSES TISSUE-DEPENDENT IRON HOMEOSTASIS ALTERATIONS: IMPLICATIONS FOR FRIEDREICH ATAXIA

Friedreich Ataxia (FA) is a cardio-neurodegenerative disease caused by mutations in the frataxin gene, which result in low frataxin expression. It is well-established that frataxin deficiency affects iron homeostasis, but the tissue-specificity of these alterations is poorly understood. In this study, we have analyzed iron homeostasis alterations in the FXNI151F mouse model, which presents systemic frataxin deficiency and neurological defects resembling FA patients. Iron overload is observed in the brain from 21-week old FXNI151F mice, both males and females, and it does not further accumulate in older animals. It is also observed in livers from 39-week old mutant females, but not in males. Iron signaling is altered in all tissues: in brain and liver Iron Regulatory Protein 1 (IRP1) content is decreased, while in heart increased IRP2 and decreased specific aconitase 2 activity are observed. Remarkably, these cardiac alterations are partially restored in 39- week-old animals, suggesting that the heart is activating an iron-deficiency response to compensate for deficient iron-sulfur biogenesis. Our findings demonstrate that frataxin deficiency affects iron homeostasis in a time dependent and tissue-specific manner, and that the pathological mechanisms in FA comprise both iron accumulation and limited iron availability. Understanding this specificity is crucial for the design of iron-related therapeutic interventions aiming to improve FA symptomatology.

biochemistry↗

bioRxiv2024

Repeat-based holocentromeres of the woodrush Luzula sylvatica reveal new insights into the evolutionary transition from mono- to holocentricity

Although the centromere is restricted to a single region of the chromosome in most studied eukaryotes, members of the rush family (Juncaceae) harbor either monocentric (Juncus) or holocentric (Luzula) chromosomes. This provides an opportunity to study the evolutionary mechanisms involved in the transition to holocentricity. Here by combining chromosome-scale genome assembly, epigenetic analyses, immuno-FISH, and super-resolution microscopy, we report the occurrence of repeat-based holocentromeres in L. sylvatica. We found an irregular distribution of genes, centromeric units, and most repeats along the chromosomes. We determined the centromere function predominantly associated with two satellite DNA repeats, Lusy1 and Lusy2 of 124- and 174-bp monomer length, respectively, while CENH3 also binds satellite-free gene-poor regions. Comparative repeat analysis revealed that Lusy1 is present in most Luzula species, suggesting a conserved centromere role of this repeat. Synteny between L. sylvatica (n = 6) and J. effusus (n = 21) genomes further evidenced a chromosome number reduction in Luzula derived from multiple chromosome fusions of ancestral J. effusus-like chromosomes. We propose that the transition to holocentricity in Luzula involves: (i) fusion of small chromosomes resembling Juncus-like centromeres; (ii) expansion of atypical centromeric units; and (iii) colonization of satellite DNA for centromere stabilization.

genomics↗

bioRxiv2023

KNL1 and NDC80 represent new universal markers for the detection of functional centromeres in plants

Centromere is the chromosomal site of kinetochore assembly and microtubule attachment for chromosome segregation. Given its importance, markers that allow specific labeling of centromeric chromatin throughout the cell cycle and across all chromosome types are sought for facilitating various centromere studies. Antibodies against the N-terminal region of CENH3 are commonly used for this purpose, since CENH3 is the near-universal marker of functional centromeres. However, because the N-terminal region of CENH3 is highly variable among plant species, antibodies directed against this region usually function only in a small group of closely related species. As a more versatile alternative, we present here antibodies targeted to the conserved domains of two outer kinetochore proteins, KNL1 and NDC80. Sequence comparison of these domains across more than 350 plant species revealed a high degree of conservation, particularly within a six amino acid motif, FFGPVS in KNL1, suggesting that both antibodies would function in a wide range of plant species. This assumption was confirmed by immunolabeling experiments in angiosperm (monocot and dicot) and gymnosperm species, including those with mono-, holo-, and meta-polycentric chromosomes. In addition to centromere labeling on condensed chromosomes during cell division, both antibodies detected the corresponding regions in the interphase nuclei of most species tested. These results demonstrated that KNL1 and NDC80 are better suited for immunolabeling centromeres than CENH3, because antibodies against these proteins offer incomparably greater versatility across different plant species which is particularly convenient for studying the organization and function of the centromere in non-model species.

genetics↗

bioRxiv2022

The dual character of the inhibitory functions of CD6

T-cell membrane scaffold proteins play important roles in T cell biology, functioning as multi-functional signaling hubs. CD6 assembles a large intracellular signalosome but, unlike typical membrane-attached scaffolds like LAT or PAG, it has a sizeable ectodomain that binds a well-characterized ligand, CD166. It is unclear whether CD6 has net inhibitory or costimulatory functions or how its ectodomain influences these activities. To explore these questions, we dissected the signaling functions of the extracellular and cytoplasmic regions of CD6. We found that CD6 was delivered to the immunological synapse and suppressed T cell responsiveness in vitro wholly dependently of its cytoplasmic domain, indicating that CD6 very potently imposes tonic inhibition, acting as a structural and signaling inhibitory hub. However, the cell-intrinsic suppression of autoimmunity by CD6 in vivo was also impacted by extracellular interactions, demonstrated by the increased susceptibility of mice to experimental autoimmune encephalomyelitis after removal of the ligand binding region of the ectodomain of CD6. Our work identifies CD6 as a new class of on/off switching scaffold-receptor that constrains immune responsiveness at two speeds. First, it sets signaling thresholds via tonic inhibition, functioning as a cytoplasmic membrane-bound scaffold and, second, by cycling between signaling-enabling and signalinginhibiting ectodomain isoforms it functions as an immune checkpoint.

immunology↗

bioRxiv2022

CD5L constraints acute and systemic inflammation and can be a novel potent therapeutic agent against sepsis

The global burden of sepsis, with an estimated 49 million cases and 11 million deaths in 2017, often passes unnoticed to the general public even though it is the direct cause of nearly 20% of all deaths worldwide. This unawareness is perhaps due to misconceptions, or miscoding in the reporting of the ultimate causes of death, as in many diseases it is not the actual infectious agent that causes the biggest harm. Rather, it is the uncontrolled inflammation leading to septic shock that is the most menacing manifestation associated with many infections, and becomes deadly serious once it has passed the stage where anti-microbial drugs no longer have any effect to inactivate or destroy the pathogen. Here we show that the combined anti-bacterial and anti-inflammatory properties of the scavenger receptor cysteine-rich (SRCR) protein CD5L contribute to a remarkable therapeutic effect of the protein to fight sepsis, such that when exogenously administered in C57BL/6 mice with induced lethal-grade sepsis, it can be a very effective curative agent to treat this condition. The resistance conferred by CD5L to polybacterial-induced sepsis using the cecal ligation and puncture (CLP) model is consistent with the reported observations that CD5L physically binds and inactivates diverse species and strains of bacteria. Accordingly, our CD5L-knockout mice are significantly more susceptible to experimentally-induced mid-grade CLP than wild-type animals. We show that CD5L is centered on promoting neutrophil recruitment and activation, overall contributing to reducing the bacteria burden of the animals. However, the dramatic susceptibility of CD5L-deficient animals is not necessarily correlated only with pathogen load, as these mice are also extremely susceptible to sterile sepsis induced by nonlethal doses of LPS. Notwithstanding the observed capacity of CD5L to directly bind to a broad range of pathogens, typical of many PRRs, our evidence suggests that the anti-inflammatory properties of the protein are at least as important as its pathogen-binding potential, and can, and should, be explored to treat the deadly inflammation storm that is sepsis.

immunology↗

bioRxiv2021

Paving the way towards understanding the inflammatory pathways triggered by giant viruses in mammalian cells: effect of mimivirus-cell interactions on IκBα degradation

Even after two decades since the identification of the first giant virus, the Acanthamoeba polyphaga mimivirus (APMV), it still elude scientists. Their gigantic size and genome are unique in the whole virosphere, and many aspects of their biology are still unknown, including their possible hosts. They are cultivated in laboratories using Acanthamoeba cells as hosts, but little is known about the infectivity of these giant viruses in vertebrate cells. However, there is evidence of the possible involvement of APMV in pneumonia and activation of inflammatory pathways. Among the hundreds of prospected giant viruses members is Tupanvirus, isolated in Brazil. Its particles have a characteristically large size varying between 1.2 to 2 m and are covered by fibrils. In the present work, we aim to study the consequences of the incubation of APMV and Tupanvirus with mammalian cells. These cells express Toll-like receptors (TLR) that are capable of recognizing lipopolysaccharides, favoring the internalization of the antigen and activation of the inflammatory system. We used a lineage of human lung adenocarcinoma cells (A549) to evaluate possible effects of TLR activation by the giant viruses and if we could detect the probable cause of the said giant-virus dependent pneumonia. Our results show that APMV and Tupanvirus (TPV) activate cellular receptors related to the Toll-like 4 type-induced inflammatory response and that the A549 cells are capable of internalizing the latter virus. Therefore, this study brings new insights into the possible interactions established between mimiviruses (here represented by APMV and Tupanvirus) and members of the innate cellular immune response.

microbiology↗

bioRxiv2021

Neutralizing antibody-independent immunity to SARS-CoV-2 in hamsters and hACE-2 transgenic mice immunized with a RBD/Nucleocapsid fusion protein

The nucleocapsid (N) and the receptor binding domain (RBD) of the Spike (S) proteins elicit robust antibody and T cell responses either in vaccinated or COVID-19 convalescent individuals. We generated a chimeric protein that comprises the sequences of RBD from S and N antigens (SpiN). SpiN was highly immunogenic and elicited a strong IFN{gamma} response from T cells and high levels of antibodies to the inactivated virus, but no neutralizing antibodies. Importantly, hamsters and the human Angiotensin Convertase Enzyme-2-transgenic mice immunized with SpiN were highly resistant to challenge with the wild type SARS-CoV-2, as indicated by viral load, clinical outcome, lung inflammation and lethality. Thus, the N protein should be considered to induce T-cell-based immunity to improve SARS-CoV-2 vaccines, and eventually to circumvent the immune scape by variants.

immunology↗

bioRxiv2021

Cholesteryl Hemiazelate Induces Lysosome Dysfunction and Exocytosis in Macrophages

OBJECTIVEA key event in atherogenesis is the formation of lipid-loaded macrophages, lipidotic cells, which exhibit irreversible accumulation of undigested modified low-density lipoproteins in lysosomes. This event culminates with the loss of cell homeostasis, inflammation and cell death. In this study we propose to identify the chemical etiological factors and understanding the molecular and cellular mechanisms responsible for the impairment of lysosome function in macrophages. APPROACH AND RESULTSUsing shotgun lipidomics we have discovered that a family of oxidized lipids (cholesteryl hemiesters, ChE), end products of oxidation of polyunsaturated cholesteryl esters, occurs at higher concentrations in the plasma of two cohorts of cardiovascular disease patients than in the plasma of a control cohort. Macrophages exposed to the most prevalent ChE, cholesteryl hemiazelate (ChA) exhibit lysosome enlargement, peripheral lysosomal positioning, lysosome dysfunction and lipidosis which are irreversible. The transcriptomic profile of macrophages exposed to ChA indicates that the lysosome pathway is deeply affected and is well correlated with lysosome phenotypic and functional changes. Interestingly, the dysfunctional peripheral lysosomes are more prone to fuse with the plasma membrane, secreting their undigested luminal content into the extracellular milieu with potential consequences to the pathology. CONCLUSIONWe identify ChA not only as one of the molecules involved in the etiology of irreversible lysosome dysfunction culminating with lipidosis but also as a promoter of exocytosis of the dysfunctional lysosomes. The latter event is a new mechanism that may be important in the pathogenesis of atherosclerosis.

cell biology↗

bioRxiv2020

The 100,000 most influential scientists rank: the underrepresentation of Brazilian women in academia.

Despite the progress observed in recent years, women are still underrepresented in science worldwide, especially at top positions. Many factors contribute to women progressively leaving academia at different stages of their career, including motherhood, harassment and conscious and unconscious discrimination. Implicit bias plays a major negative role in recognition, promotions and career advancement of female scientists. Recently, a rank on the most influential scientists in the world was created based on several metrics, including the number of published papers and citations. Here, we analyzed the representation of Brazilian scientists in this rank, focusing on gender. Female Brazilian scientists are greatly underrepresented in the rank (11% in the Top 100,000; 18% in the Top 2%). Male scientists have more self-citation than female scientists and positions in the rank varied when self-citations were included, suggesting that self-citation by male scientists increases their visibility. Moreover, male scientists had more papers never cited than female scientists. Possible reasons for this observed scenario are related to the metrics used to rank scientists, since these metrics reproduce and amplify the well-known implicit bias in peer-review and citations. Discussions on the repercussions of such ranks are pivotal to avoid deepening the gender gap in science.

scientific communication and education↗

bioRxiv2020

Impact of parasitic lifestyle and different types of centromere organization on chromosome and genome evolution in the plant genus Cuscuta

SummaryThe parasitic genus Cuscuta (Convolvulaceae) is exceptional among plants with respect to centromere organization, including both monocentric and holocentric chromosomes, and substantial variation in genome size and chromosome number. We investigated 12 species representing the diversity of the genus in a phylogenetic context to reveal the molecular and evolutionary processes leading to diversification of their genomes.We measured genome sizes and investigated karyotypes and centromere organization using molecular cytogenetic techniques. We also performed low-pass whole genome sequencing and comparative analysis of repetitive DNA composition.A remarkable 102-fold variation in genome sizes (342–34,734 Mbp/1C) was detected for monocentric Cuscuta species, while genomes of holocentric species were of moderate sizes (533–1,545 Mbp/1C). The genome size variation was primarily driven by the differential accumulation of repetitive sequences. The transition to holocentric chromosomes in the subgenus Cuscuta was associated with loss of histone H2A phosphorylation and elimination of centromeric retrotransposons. In addition, the basic chromosome number (x) decreased from 15 to 7, presumably due to chromosome fusions.We demonstrated that the transition to holocentricity in Cuscuta was accompanied by significant changes in epigenetic marks, chromosome number and the repetitive DNA sequence composition.Competing Interest StatementThe authors have declared no competing interest.View Full Text

genomics↗

bioRxiv2020

Gender, race and parenthood impact academic productivity during the COVID-19 pandemic: from survey to action.

While the Coronavirus disease 2019 (COVID-19) pandemic is altering academia dynamics, those juggling remote work and domestic demands - including childcare - have already felt the impacts on productivity. Female authors are facing a decrease in papers submission rates since the beginning of the pandemic period. The reasons for this decline in women productivity need to be further investigated. Here we show the influence of gender, parenthood and race in academics productivity during the pandemic period, based on a survey answered by 3,345 Brazilian academics from various knowledge areas and research institutions. Findings revealed that male academics - especially childless ones - were the least affected group, whereas female academics, especially Black women and mothers, were the most impacted group. This scenario will leave long-term effects on the career progression of the most affected groups. The results presented here are crucial for the development of actions and policies that aim to avoid further deepening the gender gap in science. This particular situation we are facing during the pandemic demands institutional flexibility and academia should foster the discussion about actions to benefit Black scientists and academics with families in the post-pandemic scenario.

scientific communication and education↗