A daughter parasite forms through budding from the mother cell.
As budding of the daughter parasite progresses and membrane protrusion increases (yellow), the molecular safety rope (blue) lengthens.
The images were created based on electron microscopy data and processed using AI.
© UKHD
Figure EV1: Blood-stage immunofluorescence expression profile of PfSFA2 and ultrastructure expansion microscopy (U-ExM) of PfSFA1 localization.
(A) IFA of PfSFA2-smV5 expression across the asexual blood stages, stained with an anti-V5 antibody (green), an anti-PfGAP45 antibody (magenta), and Hoechst (DNA, blue). “Ring” stage with one nucleus, trophozoite stage (“Troph”) with 2, and several stages throughout schizogony, including segmentation, are shown with the number of nuclei. The minimum and maximum displayed values for the PfSFA2-V5 and PfGAP45 channels follow the “Reset” values of the first segmentation image. Scale bars: 2 µm. (B) U-ExM of PfSFA1-smV5 schizonts stained with an anti-V5 antibody (cyan), an anti-CrCen antibody (outer-CP, magenta), SYTOX (DNA, blue), and an NHS ester-conjugated dye (grayscale). Sub-z-slices of a 7-nuclei (top) and a 14-nuclei (bottom) schizont are maximally projected and shown to the left. Representative centriolar plaque regions are numbered and shown as insets to the right. Z-depth of each maximum projection is shown to the right. Scale bars: 5 µm for full schizont; 1 µm for inset.
Creationists insist that certain biological systems are too complex to have evolved. If several interacting components are required for a system to function, they label it “irreducibly complex”; if genes encode proteins that perform a particular function, they call the DNA “complex specified information”. Both are then presented as evidence that the system must have been deliberately designed by an intelligent agent.
Curiously, however, this supposedly reliable design-detection method tends to be applied only to systems that creationists find impressive or beneficial. When comparable complexity enables a parasite to invade its host, evade its defences, reproduce rapidly and cause suffering and death, the inference to design is quietly abandoned. The parasite is instead blamed on “the Fall”, “genetic degeneration” or some other evidence-free theological excuse.
But a method that gives different answers according to whether its conclusion is theologically convenient is not a method at all. If molecular complexity, functional interdependence and genetically encoded organisation really demonstrate intelligent design, then they must do so just as reliably in a malaria parasite as in a bacterial flagellum, an eye or a blood-clotting system. And that would make them evidence not merely of intelligent design, but of intelligent malevolent design.
Two recent studies have now uncovered more of the extraordinarily elaborate machinery by which malaria parasites multiply. Instead of dividing into two daughter cells in the familiar way, Plasmodium parasites repeatedly copy their DNA and multiply their nuclei within a shared cell before producing numerous daughter parasites more or less simultaneously. The process must ensure that each viable daughter receives a nucleus and the cellular structures required to invade another host cell.
In the first study, published in The EMBO Journal, researchers identified two proteins, SFA1 and SFA2, that assemble into a fibre-like molecular tether. This tether connects the centriolar plaque associated with a parasite nucleus to the apical end of a developing daughter cell. It helps to draw the nucleus into the daughter and to organise structures, including the rhoptries and subpellicular microtubules, that the mature parasite needs for invading host cells.
When the researchers removed either SFA component, nuclear DNA could still be replicated, but the orderly construction of viable daughters was seriously disrupted. Some developing parasites lacked nuclei or possessed malformed invasion structures. In the mosquito stage of the rodent malaria parasite Plasmodium berghei, loss of either protein prevented the normal incorporation of nuclei into budding sporozoites and virtually abolished the production of infectious parasites capable of reaching the mosquito’s salivary glands. In creationist language, remove one essential component and the supposedly “designed” system collapses. This is the very kind of result they usually advertise as evidence of irreducible complexity—except that, in this case, the machinery produces malaria parasites.
The second study, published in Nature Communications, revealed another layer of organisation. Using live-cell microscopy and biophysical modelling, the researchers found that the asynchronous replication of Plasmodium falciparum nuclei is best explained by competition for a limited shared supply of one or more proteins needed for DNA replication. Rather than all the nuclei attempting to replicate simultaneously, the resource is allocated sequentially. One nucleus copies its DNA while others wait for the replication machinery to become available.
Far from being inefficient, this staggered arrangement minimises the time for which the limited molecular resource lies idle. It allows the parasite to use what is available almost continuously and accelerates the production of new nuclei. The parasite therefore possesses not only interconnected structural machinery but also a remarkably economical system for scheduling access to scarce replication resources—all ultimately dependent upon genetic sequences carrying the functional information needed to produce and regulate the components.
By creationist reasoning, we should therefore conclude that an intelligent agent supplied Plasmodium with the “specified information” and interdependent molecular apparatus needed to manufacture infectious daughter parasites efficiently. That designer also arranged for the resulting sporozoites to enter a mosquito’s salivary glands, pass into a human during a blood meal, multiply inside the liver and then invade red blood cells. If complexity and efficiency identify the designer, they also identify what the designer intended the system to accomplish.
Evolutionary biology has no such theological difficulty. Natural selection does not care about human welfare: anything that helps a parasite survive and reproduce can be favoured, however harmful the consequences for its host. Moreover, SFA proteins did not appear without ancestry. Related proteins occur in other apicomplexan parasites, while members of the same wider protein family were first identified in the flagellar rootlet fibres of green algae. The evidence points towards inherited components being modified and redeployed during evolution, not a complete system being assembled suddenly by an invisible engineer.
Glossary of Terms. Apical complexThese discoveries are therefore not evidence of genuine irreducible complexity. They reveal how evolution has produced intricate, interdependent systems from pre-existing biological components. But if creationists insist upon calling such complexity evidence of intelligent design, consistency requires them to acknowledge the character of the designer their argument implies: one that has equipped a deadly parasite with exquisitely effective machinery for multiplying, invading its hosts and perpetuating human suffering.
A specialised collection of structures at the front end of an apicomplexan parasite. It helps the parasite attach to and penetrate a host cell.
Apical pole
The front end of a developing parasite, where the structures needed for invading host cells are assembled.
Apicomplexa
A large group of single-celled parasites characterised by an apical complex. It includes Plasmodium, which causes malaria, and Toxoplasma, which causes toxoplasmosis.
Apicoplast
A specialised organelle found in most apicomplexan parasites. It is descended from a photosynthetic organism acquired through ancient endosymbiosis, although it no longer carries out photosynthesis. It performs metabolic functions essential to the parasite.
Asynchronous replication
A process in which different nuclei within the same cell copy their DNA at different times rather than simultaneously. In Plasmodium, this allows limited replication resources to be used almost continuously.
Centriolar plaque (CP)
A structure associated with the parasite’s nuclear envelope that performs some of the organisational functions carried out by centrosomes in other eukaryotic cells. It helps to organise the microtubules involved in nuclear division.
Complex specified information (CSI)
A creationist term for information claimed to be both improbable and associated with a recognisable function or pattern. It has no generally accepted, independently measurable definition in biology and provides no scientific method for distinguishing evolved genetic sequences from supposedly designed ones.
Cytokinesis
The physical division of a cell’s cytoplasm and membrane to form separate daughter cells. In Plasmodium, numerous nuclei may be produced before a final cellularisation process creates many daughters at once.
Host
An organism in or upon which a parasite lives. Malaria parasites require both a vertebrate host, such as a human, and a mosquito host to complete their life cycle.
Inner membrane complex (IMC)
A system of flattened membrane sacs beneath the parasite’s outer membrane. It supports the cell, helps determine its shape and participates in movement and daughter-cell formation.
Irreducible complexity
A creationist claim that a system requiring several interacting components could not have evolved because removing one component prevents the present system from working. This ignores evolutionary processes such as modification, duplication, co-option and changes of function, through which components can acquire their present interdependence gradually.
Karyokinesis
The division of a cell nucleus. During Plasmodium proliferation, repeated rounds of DNA replication and karyokinesis can occur before the cytoplasm divides into individual daughter parasites.
Knockout
An experimental organism in which a particular gene has been disabled or deleted. By observing what subsequently fails, researchers can investigate the gene’s normal function.
Merozoite
A daughter stage of the malaria parasite that invades red blood cells. Repeated cycles of merozoite production, release and reinvasion cause the symptoms of malaria.
Microtubules
Microscopic protein tubes forming part of a cell’s internal skeleton. They help maintain cell shape, move cellular components and separate genetic material during nuclear division.
Molecular tether or rootlet fibre
The fibre-like structure investigated in the first study. It connects the centriolar plaque associated with a nucleus to the apical pole of a developing daughter parasite, helping to guide the nucleus and organise other cellular structures correctly.
Oocyst
A cyst-like stage that develops on the outer wall of a mosquito’s intestine after fertilisation. Large numbers of sporozoites are produced within it.
Plasmodium
The genus of apicomplexan parasites that causes malaria. Its complex life cycle alternates between a vertebrate and a mosquito.
Plasmodium falciparum
The malaria parasite responsible for most severe and fatal human malaria. It was used in these studies to investigate proliferation during the red-blood-cell stage.
Plasmodium berghei
A malaria parasite that naturally infects rodents and is widely used as an experimental model. It enables researchers to study stages of the parasite’s life cycle that occur inside mosquitoes and vertebrate hosts.
Rhoptries
Club-shaped secretory organelles at the parasite’s apical end. They release proteins that help the parasite attach to, penetrate and modify a host cell.
SFA1 and SFA2
Two striated-fibre-assemblin proteins that form major components of the molecular tether connecting a nucleus to the developing daughter parasite. Disabling either gene seriously disrupts the production of properly organised offspring.
Schizogony
An unusual form of asexual reproduction in which the parasite repeatedly copies and divides its nucleus before separating into numerous daughter parasites. It occurs during proliferation in vertebrate liver cells and red blood cells.
Spore
A general biological term for a reproductive or dispersal cell. Despite their name, malaria sporozoites are specialised invasive parasite stages rather than spores in the everyday fungal sense.
Sporogony
The proliferation process within a mosquito oocyst that produces thousands of sporozoites.
Sporozoite
The slender, mobile and infectious stage that travels from the mosquito’s intestine to its salivary glands. Sporozoites enter a vertebrate host during a mosquito bite and subsequently invade liver cells.
Subpellicular microtubules
Microtubules positioned beneath the parasite’s surface. They support its elongated shape and help organise the cellular machinery required for movement and host-cell invasion.
Vector
An organism that carries a pathogen from one host to another. Female Anopheles mosquitoes are the vectors of human malaria.
The two papers were acomapnied by a news release from Heidelberg University Hospital:
New Insights into Malaria Research: How Molecular Tethers and Asynchronous Replication Drive Parasite Proliferation
Researchers from Heidelberg University’s Faculty of Medicine, Harvard Medical School, and the German Cancer Research Center (DKFZ) have uncovered key mechanisms underlying the proliferation of the malaria parasite Plasmodium. The molecular processes that govern the formation of infectious daughter parasites and new nuclei are essential for parasite survival and may therefore represent targets for future antimalarial therapies. The findings have recently been published in The EMBO Journal and Nature Communications.
Malaria parasites proliferate in an unusual way. Rather than dividing into two daughter cells like human cells, they first amplify their genetic material tenfold, hundredfold, or even thousandfold before simultaneously producing a corresponding number of daughter parasites. Until now, the mechanisms controlling these processes were only partly understood. Two recently published studies by researchers from Heidelberg University’s Faculty of Medicine, Harvard Medical School, and the German Cancer Research Center (DKFZ) provide important insights into the molecular basis of this proliferation strategy and reveal how the parasite makes particularly efficient use of limited resources within infected blood cells. The findings open new perspectives for the development of future antimalarial drugs.
A daughter parasite forms through budding from the mother cell: To do this, the membrane of the mother cell (yellow) invaginates. At the same time, an elongated fiber (dark blue) forms, which, like a molecular safety rope, connects the tip of the developing daughter cell to a cell nucleus (blue; the anchor point of the safety rope on the cell nucleus is turquoise). A structure (pink) also forms on this fiber, which will later play a key role in invading host cells.
© UKHD
Growing Daughter Parasites Secure Their Nucleus with a Molecular Tether.
The first project, published in The EMBO Journal, was conducted through a close collaboration between the research groups of Professor Friedrich Frischknecht of Heidelberg University’s Faculty of Medicine and the Department of Parasitology at the Center for Infectious Diseases of Heidelberg University Hospital (UKHD), and Professor Jeffrey Dvorin of Boston Children’s Hospital and Harvard Medical School, Boston, USA. Together, the teams investigated an enigmatic structure within the malaria parasite that had previously been observed in electron microscopy images, but whose function remained unknown. The researchers identified two proteins that form this structure, creating a molecular tether that links each of the parasite new nucleuses to the tip of a budding daughter parasite. In the absence of this tether, the formation of daughter parasites within blood cells was severely impaired.
Genetically modified parasites lacking one component of the tether were still able to replicate their genomes normally but could no longer produce viable progeny. The consequences were particularly dramatic in mosquitoes, where the formation of sporozoites, the infectious stage transmitted to humans during a mosquito bite, was almost completely abolished.As budding of the daughter parasite progresses and membrane protrusion increases (yellow), the molecular safety rope (blue) lengthens, holding the cell nucleus (light blue, turquoise: anchor point) as well as other vital organelles (green, orange, pink) within the developing parasite.© UKHD
Without this connecting structure, the entire process of daughter parasite formation collapses. The developing parasites are unable to pull their nucleus inside and cannot orient cellular structures correctly that are important for host-cell invasion. These Plasmodium parasites are not viable.
Professor Friedrich Frischknecht, co author of the EMBO Journal paper.
Department of Parasitology
Center of Infectious Diseases
Medical Faculty
Heidelberg University
Heidelberg, Germany
A Limiting Protein Resource Coordinates Nuclear Multiplication.
In the second project, recently published in Nature Communications, the researchers investigated how parasite nuclei are generated. For this study, the group of Dr. Markus Ganter of Heidelberg University’s Faculty of Medicine and the Department of Parasitology at UKHD collaborated with scientists from Heidelberg University’s Institute for Theoretical Physics and BioQuant Center, as well as the Division of Theoretical Systems Biology at DKFZ led by Dr. Nils Becker. During the blood stage of infection, the malaria parasite multiplies its nuclei through an unusual asynchronous process, despite residing in a shared cell. While one nucleus may be replicating its genome, a neighbouring nucleus may already be undergoing division. Using high-resolution live-cell microscopy and mathematical modelling, the researchers demonstrated that the nuclei compete for a shared and limiting protein resource required for genome replication. As a result, the nuclei replicate their genomes at different times. While one nucleus gains access to this limiting protein resource and duplicates its genetic material, the remaining nuclei must wait until the resource becomes available again. That way, asynchronous nuclear multiplication can be established within the parasite.
Unexpectedly, this system does not slow parasite proliferation. On the contrary, mathematical modelling and experimental validation showed that available resources are used with virtually no idle time, allowing the parasites to proliferate particularly efficiently and even somewhat faster than would be possible if all nuclei replicated in a fully synchronized manner.
If all nuclei were to duplicate their genomes simultaneously, they would have to share the available protein resources, which would ultimately slow down the process.
Dr. Ganter, co-corresponding author
Center for Infectious Diseases—Parasitology
Medical Faculty
Heidelberg University
Heidelberg, Germany.
[Dr. Ganter] carried out his earlier research together with Jeff Dvorin during their time together as postdoctoral fellows at the Harvard T.H. Chan School of Public Health. Highly Specialized Proliferation Mechanisms May Prove to Be an Achilles’ Heel
Malaria parasites have evolved highly specialized strategies to reproduce as rapidly and efficiently as possible. These unusual mechanisms may prove to be their Achilles’ heel. The better we understand them, the more precisely we can identify new targets for future drug development.
Professor Friedrich Frischknecht.
Currently used antimalarial drugs interfere with parasite multiplication in blood cells, while some also target parasites in the liver. However, the pathogens adapt rapidly and frequently develop drug resistance.
Malaria parasites proliferate both in humans and in the mosquito vector. In humans, a single parasite inside a liver cell can generate a population of many tens of thousands of offspring that subsequently disperse and infect red blood cells. Within red blood cells, each parasite produces approximately 30 daughter parasites. In mosquitoes, the parasite undergoes extensive multiplication within cyst-like structures in the wall of the mosquito intestine. A single parasite can give rise to around 5,000 offspring, which migrate to the salivary glands and are transmitted to a human host during the mosquito’s next blood meal.
Publications:He, B., Ali, I., Dorner, L.P. et al.
Essential nucleus-apical pole linkage maintains division fidelity during Plasmodium progeny formation. EMBO J 45, 5388–5422 (2026). https://doi.org/10.1038/s44318-026-00836-7
Binder, P., Kudulytė, A., Klaus, S. et al.
Competitive resource allocation drives asynchronous and rapid nuclear multiplication in the malaria parasite. Nat Commun 17, 7413 (2026). https://doi.org/10.1038/s41467-026-75378-x
What these two studies reveal, then, is not merely another layer of complexity in the life cycle of Plasmodium, but exactly the combination of specialised proteins, coordinated processes and functional genetic information that creationists routinely present as evidence of intelligent design. Remove a critical component of the molecular tether and the production of viable infectious parasites collapses; disrupt the coordination of nuclear replication and the parasite loses the efficiency with which it exploits its host’s limited resources. By creationist standards, these systems should qualify as exhibits for both “irreducible complexity” and “complex specified information”.
The problem is that their function is not to benefit humanity. It is to manufacture thousands of infectious parasites, deliver them to a mosquito’s salivary glands, inject them into another host and enable them to invade liver cells and red blood cells. If functional complexity proves design, then the supposed designer did not merely permit malaria to exist: it furnished the parasite with the molecular machinery needed to spread, proliferate and cause disease with remarkable efficiency.
Creationists cannot escape that conclusion by invoking “the Fall”. No evidence shows that these structures were once designed for some harmless purpose and later became corrupted. They are specialised components of an integrated life cycle involving both vertebrate and mosquito hosts. Moreover, claiming that mutation and degeneration transformed something benign into such an elaborate and effective parasitic system would concede the very point creationists normally deny: that inherited variation and natural selection can generate new functions, new interactions and complex biological information.
Evolutionary biology explains the findings without inventing either a benevolent or a malevolent supernatural engineer. Plasmodium inherited cellular components from its ancestors and, over immense periods, natural selection modified and redeployed them. Variants that packaged daughter parasites more reliably, used replication proteins more economically or reached the next host more successfully left more descendants. Natural selection has no foresight, conscience or concern for human suffering; it preserves whatever increases reproductive success in the organism concerned.
The researchers therefore had no need to insert magic into the remaining gaps in their knowledge. They investigated the proteins, altered the relevant genes, observed the consequences and constructed testable models of the replication process—all within the evolutionary framework that makes sense of both the parasite’s complexity and its harmfulness.
Creationists cannot have it both ways. Complexity cannot be the unmistakable signature of their god when it inspires admiration but cease to indicate design when it produces suffering and death. Either these malaria systems evolved, in which case “irreducible complexity” and “specified information” are not evidence of design, or they were deliberately designed, in which case the evidence points not towards a loving creator but towards an intelligent and extraordinarily inventive malevolence.
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