Women scientists work in a laboratory with a microscope and test tubes.

From Stepping Aside to Stepping Forward

Women in science have come a long way, and they do not intend to stop.

In the mid-1990s, Nancy Hopkins, a biologist and tenured faculty member at the Massachusetts Institute of Technology (MIT), realized that she had been allocated less lab space than her male colleagues, so she turned to a trusted friend: data. She measured every inch of her lab to irrefutably prove the inequitable distribution of space. Along the way, she teamed up with her fellow women faculty members to address other aspects of gender bias at the institution. In their investigation, they found that senior women faculty felt invisible, were excluded from positions of power, and received fewer resources and rewards than their male counterparts. Their report, published in 1999, was instrumental in bringing about a change in MIT policies to improve the status of women faculty.

Despite the changing landscape, gender disparity in academia still exists. This is in the spotlight now because March is National Women’s History Month, but I believe that efforts to support women in science should be perpetual, not restricted to a celebratory month or day. However, this occasion presents an excellent opportunity to share the stories of exemplary women, track ongoing progress, and take action to aid and inspire the current and next generation of women scientists. 

At The Scientist, we want to celebrate women in science in all ways. Throughout the month, we will highlight stories that feature women scientists on our social media platforms. For the month of March, we are also accepting nominations of exceptional women scientists—your colleagues, friends, role models, or yourself—through our “Peer Profile” program. Just tell us who we should cover, what they work on, and why you find them so amazing. We look forward to your nominations!

Nominate a woman scientist


  1. Chisholm SW, et al. MIT Faculty Newsletter, Special Edition: A Study on the Status of Women Faculty in Science at MIT. 1999. Issue 4, Vol. 11.
The illustration shows adipocytes, cells of the adipose tissue, and Trypanosoma brucei parasites that occupy the extracellular spaces between the cells.

Lose the Fat and Curb Parasitic Infection

Trypanosoma brucei infection induces fat breakdown, but this strategy benefits the host. 

Trypanosoma brucei (T. brucei) enters its host’s body through the painful bite of infected tsetse flies, causing sleeping sickness, which can be fatal if left untreated. In her laboratory at the University of Lisbon, parasitologist Luísa Figueiredo studies the mechanisms underlying T. brucei infections.

Her team previously found that T. brucei accumulates in large amounts in the adipose tissues of mice, where it undergoes changes in its ability to uptake and metabolize lipids.1 This observation, combined with the fact that Trypanosoma infections induce fat loss, led the team to hypothesize that the parasite alters lipid metabolism in adipose tissue.

          The photo shows a mixture of normal and atrophied adipocytes (white circles), T. brucei parasites (brown), and the nucleus of infiltrated immune cells (blue).
Adipose tissue serves as a reservoir for T. brucei parasites. The parasites (shown in brown) accumulate outside the adipocytes (white circles).
Tânia Carvalho

In their recent Nature Microbiology paper, the team reported that T. brucei stimulates lipolysis in fat cells by modulating the host enzyme that initiates this process. They also found that this response counterintuitively benefits the host, opening avenues for novel treatment strategies.

To uncover how the parasite induces fat loss, the researchers used wildtype and knockout mice that lacked adipocyte triglyceride lipase (ATGL), a key enzyme in lipolysis, in their adipose tissues. When infected with T. brucei, wildtype mice lost adipose tissue and had higher levels of fatty acids (FFA), a product of lipolysis. Despite preserving fat mass during the infection, ATGL-deficient mice had shorter lifespans and higher parasite loads in their fat tissues than their wildtype counterparts.

After identifying the FFA from the adipose tissues of wildtype mice and testing them on the parasite in vitro, the researchers were surprised to find that one fatty acid killed, rather than benefitted, the parasite.        

“It had often been thought that the wasting associated with these infections was a consequence of high parasitemia,” said Monica Mugnier, a T. brucei researcher at Johns Hopkins University who was not involved in the research. “This result shows that the fat loss may actually be a protective mechanism during the infection.”


  1. Trindade S, et al. Cell Host Microbe. 2016;19(6):837-848.
  2. Machado H, et al. Nat Microbiol. 2023;8(11):2020-2032.
3D rendered single cell next to a cluster of cells, illustrating the concept of stem cell differentiation and proliferation.

Selecting Cytokines for Organoid Cultures

Scientists optimize organoid culture growth and consistency with validated growth factor panels.

Organoids hold the key to unlocking 3D discoveries in disease and development. Whether researchers aim to model organ architecture1 or replicate tumor microenvironments,2 growing and differentiating stem cells into specific organoids starts with choosing the right protocols and reagents.

          Human body diagram with inset organoid types connected to target tissues (mammary gland organoid, liver organoid, intestinal organoid, cerebral organoid, lung organoid, and stomach organoid).
Researchers use different combinations of cytokines to culture a variety of organoids.
Sino Biological

Scientists introduce cytokines and growth factors into culture media to manipulate the signaling pathways involved in organoid formation. Different combinations can be used to culture almost all organoids, including gastric epithelial organoids, liver organoids, pancreatic organoids, and breast organoids. The cytokine mixture required depends on the stem cell source and developmental pathways of the target tissue.3 For example, WENR (Wnt3a/EGF/NOG/RSPO1)1 is one of the most classical cytokine schemes for intestinal organoid cultures, and this scheme can also be applied for other target tissues.

Wnt signaling governs several aspects of development, including cell fate determination, cell migration and proliferation, and tissue maintenance and regeneration.4 In organoid cultures, Wnt signaling helps kickstart tissue formation. Along with epidermal growth factor (EGF), Noggin (NOG), and R-spondin (RSPO1), Wnt allows scientists to culture stem cell-enriched organoids.1 Other critical components that promote stem cell growth and differentiation in organoid cultures include bone morphogenetic protein (BMP) and fibroblast growth factor (FGF).3

Researchers can optimize organoid culture growth and consistency with panels of growth factors that are specifically validated for organoids, such as the WENR cytokines developed by Sino Biological. Growth factor panels have reliable bioactivity and batch-to-batch consistency, enabling scientists to dependably grow organoids representative of their desired target tissues.

Learn more about panels of growth factors for organoid culture.


  1. Boonekamp KE, et al. J Mol Cell Biol. 2020;12(8):562-8.
  2. Sun CP, et al. Front Immunol. 2022;13:770465.
  3. Lancaster MA, Knoblich JA. Science. 2014;345(6194):1247125.
  4. Mehta S, et al. Front Cell Dev Biol. 2021;9:714746.
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front view of a green grasshopper with a white and orange face.

Why Do Male Organisms Exist?

Some species of lizards, grasshoppers, and crustaceans have adopted a ladies-only lifestyle.

In recent years, more and more instances of parthenogenesis have emerged as “virgin births” in crocodiles, condors, and king cobras. While these animals can create babies without males in a pinch, a few other species have fully committed to parthenogenesis, going male-free for more than a million years.1

“There are a lot of advantages to getting rid of males and just reproducing by parthenogenesis,” said Michael Kearney, a physiological ecologist at the University of Melbourne. “The most powerful one is that everybody in the population is producing offspring, so the population growth rate doubles.” Parthenogenesis also protects animals from the dangers of sex, including exposure to predators and sexually transmitted infections.

At least in the short-term, this can be a highly successful strategy: Warramaba virgo, an all-female grasshopper species, hasn’t had sex in a quarter million years and appears to be thriving.2 Although single nucleotide polymorphism analysis revealed much less genetic variation in W. virgo compared to closely related sexual species, when Kearney and his colleagues investigated 14 fitness-related traits, including heat and cold tolerance, reproductive output, and longevity, they found that the parthenogens were on par with their sexually-reproducing relatives.

And yet, said, Kearney, “We don't see really old parthenogens, so something gets them in the end.” 

“Sex mixes things in a particular way, bringing together new combinations of genes that might be advantageous,” he said. This might help animals cope with changing environments and rapidly evolving pathogens. And indeed older parthenogenic species may feel these costs: Some parthenogens have higher parasite loads, fewer positively selected genes, and a faster accumulation of deleterious mutations than their sexually-reproducing relatives.3,4 

However, Kearney noted that the mystery isn’t completely solved. “There are still interesting questions about how the genomes of parthenogens evolve, and to what extent that can help create diversity and maybe even meaningful phenotypic diversity.”

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  1. Schwander T et al. Curr Biol. 2011;21(13):1129-1134.
  2. Kearney MR et al. Science. 2022;376(6597):1110-1114.
  3. Moritz C et al. Proc Royal Soc B. 1991;244(1310):145-149.
  4. Jaron KS et al. Sci Adv. 2022;8(8):eabg3842.

Predict Functional Genomics with Confidence

An advanced multiomics solution allows researchers to predict gene expression, chromatin accessibility, and enhancer state from one DNA sample.

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The First Human Embryo Model From Embryonic Stem Cells

Jacob Hanna developed a method for replicating embryogenesis outside of the uterus to understand the underlying mechanisms.

          Fluorescent microscopy image of an embryo model representing four tissue layers of this developmental stage. Cyan-labeled cells are clustered at the top of an ovoid structure, underneath them are yellow-labeled cells and under them red-labeled cells, and surrounding all three layers are white labeled cells.
Embryo models could help scientists understand stem cell differentiation, the development of organs, and how defects arise. Scientists imaged this embryo model after eight days in culture. It consists of four tissue structures: epiblast (cyan), yolk sac (yellow), extra-embryonic mesoderm cells with early chorionic cavity (red), and trophoblast layer (white).
Jacob Hanna

During embryonic stem cell (ESC) development, pluripotent stem cells transition from a naïve state into a primed state before they take their first steps toward a lineage commitment. Jacob Hanna, a stem cell biologist at the Weizmann Institute of Science, wanted to know why this transition occurs. To answer this question, Hanna and his team set out to develop an ex utero embryo model. 

Hanna recognized that the project was ambitious and could not be rushed. So, his team first studied the conditions for growing a normal embryo from a mouse outside of the uterus.1 Then they identified the cell types and conditions needed to develop a murine embryo from mouse embryonic cells.2 Finally, they developed the first human embryo model created from naïve human ESC.3  “It took a lot of iterations and trials,” Hanna said. 

The team differentiated the human naïve ESC into four subpopulations and cultured them at specific ratios to promote the development of embryonic tissues. While monitoring the ESC-based embryo model’s growth for important structures, they captured an image eight days after culture that included the epiblast, yolk sac, extra-embryonic mesoderm, and trophoblast. The team used atlases to compare the structures of their model to normally developed embryos

While some researchers anticipate studying embryos beyond the 14-day limit, Hanna stressed the importance of having a high quality model over longer culture periods. “It’s not about counting days; it’s about getting an embryo that looks like what it should,” Hanna emphasized.

According to Hanna, these models will help answer how a primed state benefits cell differentiation, understand developmental errors that lead to nonviable pregnancies, and improve organ development for transplantation.  


  1. Aguilera-Castrejon A, et al. Ex utero embryogenesis from pre-gastrulation to late organogenesis. Nature. 2021;593:119-124
  2. Tarazi S, et al. Post-gastrulation synthetic embryos generated ex utero from mouse naïve ESC. Cell. 2022;185(18):3290-3306
  3. Oldak B, et al. Complete human day 14 post-implantation embryo models from naïve ES cells. Nature. 2023;622:562-573
Abstract illustration depicting coronavirus research concept.

Curiosity and Compassion Fuel Rare Disease Research

Lauren Drouin shares how personal connections and scientific curiosities drive her work on gene therapy viral vectors. 

Lauren Drouin is the director of analytical development and the Genomic Medicine Unit at Alexion AstraZeneca Rare Disease. As a dynamic scientist with unique expertise in current research and industry trends for gene therapies, Drouin is passionate about driving progress within the rare disease field and advancing products from preclinical development into the clinic and beyond.  

In this Science Philosophy in a Flash podcast episode brought to you by Bio-Rad, The Scientist’s Creative Services Team spoke with Drouin to learn more about her interest in adeno-associated virus (AAV) biology, and what motivated her journey from academia to patient-focused analytical development research.

          Headshot of Lauren Drouin.

Lauren Drouin, PhD
Director, Analytical Development
Genomic Medicine
Alexion Pharmaceuticals 
AstraZeneca Rare Disease

Learn more about Lauren Drouin and developing viral vectors.

Learn More
<style type="text/css" >p.p1 {margin: 0.0px 0.0px 0.0px 0.0px; font: 13.8px Helvetica; color: #000000}</style>Purple cartoon of candida auris with lines pointing places the bacteria clings to in a hospital, like a wheelchair, bed, skin, and catheter.&nbsp;

Seeking Solutions for a Sticky Situation

To cling to everything from catheters to skin, Candida auris uses a unique approach.

In 2009, Candida auris appeared seemingly out of nowhere.1 Since then, its rapid emergence in hospitals and extreme drug resistance has earned this pesky pathogen a spot on both the CDC and WHO high threat lists.2,3 Its success likely comes from its ability to persistently stick to surfaces, but how it does this was unclear. Recently, researchers discovered the clingy culprit, a new, uncharacterized protein, which they hope will inform new therapeutics.4 

Teresa O’Meara, a geneticist at the University of Michigan and author of the paper published in Science, started the investigation by probing the obvious offenders: 12 conserved adhesins, proteins that fungal pathogens use to stick to surfaces. “We really thought that one of these would be important,” said O’Meara. “It turns out that not really.” To expand their search, the researchers screened more than 2,000 C. auris mutants in search of one with limited clinging capacity. This led them to an unknown adhesin: Surface Colonization Factor 1 (Scf1). 

“What stands out is how strong the phenotypes are of this gene,” said Christina Cuomo, a fungal geneticist at Brown University who was not involved in the study. Although many adhesins are conserved across Candida species, Scf1 isn't, and only C. auris required Scf1 to stick to surfaces. 

O’Meara and her team discovered that, unlike other adhesins, the exposed N-terminal domain of Scf1 is enriched with cationic amino acids, which facilitate an incredibly strong bond— second only to covalent bonds—with certain surfaces. Mollusks and barnacles use a similar approach to cling tightly to rocks.

O’Meara’s team further demonstrated Scf1’s role in infections. C. auris strains lacking SCF1 exhibited reduced catheter and skin colonization in rodent and ex vivo human skin explant models, whereas overexpression of the gene drove this behavior. “What was really shocking to us was that it’s actually required for causing disease,” said O’Meara, who hopes to further probe the novel adhesin’s behaviors during infection in future experiments.


  1. Satoh K, et al. Microbiol Immunol. 2009;53(1):41-44.
  2. CDC. Department of Health and Human Services, CDC. 2019. 
  3. WHO. World Health Organization. 2022.
  4. Santana DJ, et al. Science. 2023;381(6665):1461-1467.
An automated pipetting instrument dispenses green liquid into a clear 96-well plate.

Breaking Down Barriers to Single-Cell Resolution

Microfluidic digital dispensing technology can gently isolate viable and healthy cells suitable for a range of downstream applications.

Cellular heterogeneity drives many physiological and pathological responses, but conventional analysis methods that sample only in the aggregate can mask signal from rare cell types.1,2 Achieving single-cell resolution has revolutionized scientists’ understanding of cellular behavior, function, and characterization, helping them advance in many fields.2 However, isolating and separating individual cells for downstream single-cell applications can be technically challenging.

     An Uno Single Cell Dispenser instrument, viewed from the side, on a white background.
The Uno Single Cell Dispenser is a benchtop device designed to lower barriers to entry for scientists looking to access single-cell resolution.

Numerous techniques for single-cell separation, isolation, and sorting exist, ranging from manual manipulations to high-throughput instruments capable of processing tens of thousands of cells. In all of these, the primary considerations are yield, quality, purity, throughput, and accessibility.2 Techniques that rely on manual manipulation, such as limiting dilution, do not require sophisticated instruments, but are inefficient and less accurate. Conversely, fluorescence activated cell sorting (FACS) offers high throughputs, but requires complex instrumentation, can be difficult to master, and applies significant mechanical force upon the cells.2

Microfluidics offers a potential third option to this dichotomy. Microfluidic devices separate cells by passing cellular suspensions through microchannels into distinct chambers, thereby providing throughput and accuracy without exerting mechanical stress upon cells.2 While earlier microfluidic devices were complex and highly specialized, newer models are designed with lowering barriers to entry in mind.3 Instruments like the benchtop Uno Single Cell Dispenser™ focus on lower costs, smaller footprints, and greater user-friendliness. None of this comes at the expense of functionality. For example, the Uno can provide 384-well throughput in five minutes with picoliter-level accuracy.Microfluidic digital dispensing technology can gently isolate viable and healthy cells suitable for a range of downstream applications including mass spectrometry-based single-cell analysis, stem cell libraries, 3D cell research, and cell line development.

Read more about microfluidic digital dispensing technology.


  1. Hu P, et al. Front Cell Dev Biol. 2016;4:116
  2. Gross A, et al. Int J Mol Sci. 2015;16(8):16897-919
  3. Sanchez-Avila X, et al. J Am Soc Mass Spectrom. 2023;34(10):2374-80
  4. Uno Single Cell Dispenser™. Tecan Life Sciences. 2023.
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A researcher looks at the screen of an imaging equipment. She sees a picture of a Western blot membrane.

The Mysterious Western Blot Message

Elissavet Chartampila meticulously crafted handwritten labels for her lab tools. Little did she know that some labels last forever.

          A young woman wears a blue sweater with UNC written on it and smiles at the camera.
Elissavet Chartampila, a neuroscience graduate student at the University of North Carolina at Chapel Hill, studies the roles of sleep in development and neurodevelopmental disorders like autism and schizophrenia using animal and in vitro models.
University of North Carolina at Chapel Hill

I joined the University of North Carolina at Chapel Hill in 2021 as a neuroscience graduate student. That fall, I rotated in Graham Diering’s lab, focusing on the role of sleep on normal development and the effects of its disruption on neurodevelopmental disorders such as autism. 

One of the first techniques I learned was western blot, which I planned to use to test if a viral method could knock down a scaffolding protein in cell cultures. One day, towards the end of my rotation, I took my western blot membrane to the imaging equipment to analyze the results of a key experiment. When I glanced at the instrument screen, I was confused to see the words “gel transfer” imprinted vertically in the middle of the membrane. 

I investigated the potential cause for the message over the next few days, but my efforts ended up being unsuccessful. I decided to move on and redo the experiment since I fortunately had enough samples to try again. 

As I prepared to repeat the gel transfer step, I noticed an intriguing detail: The conical tube I used to roll the gel onto the membrane had the words “gel transfer” written on it. I had created this label to identify this tube as my dedicated western blotting tool. Then it dawned on me: The handwriting that mysteriously appeared on my earlier experiment was mine, and it probably appeared there because I inadvertently touched the membrane to the label on the tube. The realization of this was an amusing "aha" moment that put the origin of the mysterious message to rest.

Western blotting is a technique where many things can go wrong. Paradoxically, my mistake boosted my confidence for using this technique in my following research experiments. The handwritten label on my conical tube is gone. Now, I just place my unlabeled western blot tube with the other western blot tools in my drawer. 

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Test tubes in laboratory, 96 microwells microplate with ABTS

AI-Powered Automation: Revolutionizing 3D Cell Culture

Researchers streamline cell culture with automated systems, incorporating machine learning to save time and improve reproducibility.

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Scientists create 3D cell culture models such as organoids, spheroids, and organs on a chip for molecular biology research and high throughput drug discovery.1 Unlike costly animal models or 2D cell culture systems that inadequately represent multifaceted tissues, 3D cell culture models are more financially accessible for in-depth biological studies and enable scientists to recapitulate complex physiological functions. However, the culturing process behind models such as organoids is highly involved, often requiring multistep manual methods that are time consuming, laborious, and subject to reproducibility challenges.1

     A 3D rendered image of the CellXpress.ai Automated Cell Culture System in a laboratory.
The CellXpress.ai Automated Cell Culture System automates 3D biology, improves workflows, and makes assays more reliable and reproducible.
Molecular Devices

Conventional methods for 3D cell culture rely on human intervention across all steps of growth, including seeding stem cells, collecting aggregates, feeding differentiating cells long term, and imaging and tracking cultures as they grow. Automated cell culture systems that incorporate liquid handling, incubation, monitoring, and imaging optimize these protocols.1

Recent tools that connect automation and artificial intelligence (AI)-mediated feedback systems further optimize this process by modulating culture conditions and screening data with minimal human input.2 For instance, machine-learning algorithms can efficiently monitor and instruct automated technologies for efficient organoid construction, image analysis, and application readouts. AI reduces hands-on time in the laboratory and limits opportunities for human error and variability.1,2

New AI-enabled automation technologies, such as the CellXpress.ai™ Automated Cell Culture System from Molecular Devices, improve high-throughput cell culture reliability and reproducibility, which is particularly important for 3D culture workflows and drug development.3 This allows researchers to scale up their cell culture models, facilitating faster and more relevant discoveries.

Read more about AI-driven automated cell culture.


  1. Louey A, et al. SLAS Discov. 2021;26(9):1138-47.
  2. Bai L, et al. Bioact Mater. 2024;31:525-48.
  3. CellXpress.ai Automated Cell Culture System. Molecular Devices. 2023.
Small brown and white fat-tailed dwarf lemur on a white background.

Do Animals in Warm Climates Hibernate?

Animals that wind down in the tropics may take us to new frontiers in organ preservation.

          Kathrin Dausmann releasing a fat-tailed lemur from a silver box.
Kathrin Dausmann, an ecologist at the University of Hamburg, travels to field sites in Madagascar to study tropical hibernators, such as the fat-tailed dwarf lemur.
Kathrin Dausmann, Julian Glos

The term hibernation evokes images of plump bears curled up in cozy dens to survive winter. But these aren’t the only places to find slumbering critters. 

Earlier in her career, Kathrin Dausmann, an ecologist at the University of Hamburg, became perplexed while running fieldwork in Madagascar. “We had a very cute species in the forest that nobody knew what they did during winter. They just were gone,” she said. Eventually, Dausmann found the adorable fat-tailed dwarf lemur hibernating in tree holes and underground chambers.1,2 

During hibernation, animals slow their metabolisms and match their internal body temperatures to ambient conditions. Whether tropical hibernators—primates in particular—use similar cellular and molecular mechanisms as cold-weather animals to regulate this state of suspended animation remains largely unknown. “We lag behind 50 years of hibernation research in the tropical areas,” said Dausmann. 

To change that, Ken Storey, a molecular physiologist at Carleton University, ran a series of studies in the grey mouse lemur, a warm weather primate. In one study comparing lemurs in and out of hibernation, he measured changes in the expression of genes that scientists previously identified to regulate hibernation in arctic ground squirrels.4 Relative to awake controls, hibernating lemurs exhibited an upregulation in only a selection of the genes, which primarily occurred in the liver and brown fat. Storey also observed tissue-specific, differential activation of the mitogen-activated protein kinase (MAPK) signal transduction and insulin signaling pathways, elevations in heat shock proteins and antioxidant enzymes, an upregulation in microRNA implicated in cell development and survival pathways, and a downregulation in microRNA targeting immune function.5-8

Understanding the molecular drivers of hibernation, especially in primates, could provide new solutions for organ preservation. Rather than cooling organs, which can cause damage, exploiting strategies that tropical hibernators use to maintain organs at nearly normal physiological levels could extend the transplant timeline.9 

What makes you curious? Submit a question for us to answer in future “Just Curious” columns.

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  1. Dausmann KH, et al. Nature. 2004;429(6994):825-826.
  2. Blanco MB, et al. Sci Rep. 2013;3:1768.
  3. Mohr SM, et al. Annu Rev Cell Dev Biol. 2020;36:315-338.
  4. Biggar KK, et al. Genomics Proteomics Bioinformatics. 2015;13(2):111-118.
  5. Biggar KK, et al. Genomics Proteomics Bioinformatics. 2015;13(2):81-90.
  6. Tessier SN, et al. Genomics Proteomics Bioinformatics. 2015;13(2):91-102.
  7. Wu C-W, et al. Genomics Proteomics Bioinformatics. 2015;13(2):119-126.
  8. Biggar KK, et al. Gene. 2018;677:332-339.
  9. Hadj-Moussa H, Storey KB. FEBS J. 2019;286(6):1094-1100.
3D illustration of Leishmania parasite against a black background.

Survival of the Fittest Parasite

Ever the resourceful parasite, Leishmania co-opts a natural antibody from blood to breed.

          ]: A colorized image of parasite clumps from a scanning electron microscope.
Researchers used a scanning electron microscope to visualize Leishmania parasite clumps (colorized).
Vinod Nair, Rose Perry-Gottschalk, and Ana Barletta

After sandflies feast on blood from a vertebrate host, Leishmania parasites mate and multiply within their guts. Leishmania mainly reproduces asexually but can fuse to form hybrids and swap genes between parasites.¹ However, factors that mediate genetic exchange are poorly understood. In a recent Nature paper, researchers reported that Leishmania uses vertebrate host antibodies from the sandflies’ blood meal to mate, unveiling a new paradigm in parasite-vector-host interactions.² 

Jesus Valenzuela, a biochemist at the National Institute of Allergy and Infectious Diseases, and his team cocultured two Leishmania strains in media containing sera from more than ten different vertebrates, including adult humans, to recapitulate the sandfly’s meal. They observed the formation of spherical Leishmania mating clumps (LMC), which facilitated genetic exchange, in all parasites except those cultured in the standard culture medium containing fetal bovine serum. 

When Valenzuela analyzed the different sera, he noted that they all contained IgM natural antibodies (IgMn). Without IgMn, the LMC failed to form. Further characterization showed that IgMn bound to Leishmania to facilitate fusion, genetic exchange, and eventual dissociation to release new parasites. 

“It’s an unexpected way to facilitate genetic exchange, but this work pinpointed these natural IgM antibodies as a critical factor,” said Nathan Peters, an immunologist at the University of Calgary who was not involved in the study. “It’s fascinating how the parasites use these defense mechanisms in their favor.”

Gene transcription analysis of the parasite clump revealed that IgMn upregulated proteins involved in cell fusion and division. The team also confirmed their findings in vivo by controlling the IgMn intake of sandflies. Sandflies on a consistent IgMn diet showed a 12-fold increase in LMC compared to control sandflies fed blood without IgMn.

“It’s a perfect storm,” said Valenzuela. To reproduce, “You need to have these three elements together. It begins with the inside of the vector, the presence of the parasite, and the parasite using IgMn from the blood meal in the sandfly gut.”


  1. Akopyants NS, et al. Science. 2009;324(5924):265-268.
  2. Serafim TD, et al. Nature. 2023;623(7985):149-156.
Image of plant cells with chloroplasts (lilac) expressing the protein huntingtin (green).

Greening the Fight Against Huntington’s Disease

Plant chloroplasts offer insights for shielding against protein aggregation in Huntington’s disease.

          Ernesto Llamas smiling as he sits at the lab bench with Arabidopsis plants.
Ernesto Llamas, a plant biologist at the University of Cologne, studies how Arabidopsis thaliana plants actively remove harmful protein aggregates and avoid their harmful effects.
Jenny Fenger

Plants and humans are different in many ways, but they share some commonalities. For instance, plants express hundreds of proteins containing polyglutamine (polyQ) regions.¹ Humans express similar proteins, but in humans their buildup causes neurodegenerative diseases like Huntington’s disease. Understanding plants' survival holds therapeutic promise for protein aggregation related diseases, according to Ernesto Llamas, a molecular biologist at the University of Cologne. 

Llamas and his team sought to identify the mechanism that renders plants immune to toxic protein aggregation. In a paper published in Nature Aging, Llamas described a chloroplast protein that shields plants from the harmful effects of polyQ proteins.² His findings hint at the use of chloroplast proteins as unconventional future therapies for polyQ diseases. 

Llamas grew genetically modified Arabidopsis thaliana plants to express low (28 glutamine) and high (69 glutamine) repeat levels of human huntingtin protein, where greater than 35 glutamine repeats trigger polyQ aggregation. Llamas expected to see aggregates, but to his surprise, the plants developed normally. 

“Plants have a principal characteristic: chloroplasts,” said Llamas. “This extra organelle contains expanded molecular machinery to deal with toxic protein aggregates.”

When he analyzed plant-human protein interactions, one caught his eye: polyQ proteins bound to a chloroplast-specific protein called stromal processing peptidase (SPP). Chloroplasts imported and degraded polyQ proteins; when the team disrupted the chloroplasts, this clean-up machinery ceased.

Llamas wanted to transfer SPP’s protective ability to human cells. He cotransfected human cells to overexpress polyQ containing proteins and to express SPP. Microscopy and protein measurements showed that SPP reduced protein aggregation compared to cells with polyQ aggregation that did not express SPP.

“It is a big discovery to express plant SPP in their experimental models,” said Piere Rodriguez Aliaga, a biophysicist at Stanford University who was not involved in the study. “The therapeutic effect is there, but the off-target effects [with other proteins] are still a puzzle that needs to be solved.”

Moving forward, Llamas is optimistic about the therapeutic potential of harnessing the protective power of chloroplasts.


  1. Kottenhagen N, et al. Proc. GCB. 2012;26:93-107.
  2. Llamas E, et al. Nat Aging. 2023;3:1345-1357.
March Digest crossword image

Science Crossword Puzzle

Put on your thinking cap, and take on this fun challenge.