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Mallick, S.

Publications and source records attributed to Mallick, S..

At least 19 recordsLinked to original sources

Microrobot and Cellbot Locomotion in Confined Hydrogels and Cardiac Tissue Surfaces

Biohybrid cellbots and microrobots are a promising platform for targeted drug delivery, minimally invasive surgery, and tissue engineering. Here, we present a comparative analysis of the locomotion dynamics across synthetic substrates and ex vivo cardiac tissue to help bridge the gap presented by translating locomotion dynamics from idealized environments to biological interfaces. By subjecting the microrobots and cellbots to different substrates (specifically, cell culture dish, hydrogel, and ex vivo tissue) and applying rotating magnetic fields at varying frequencies, we characterized how surface boundary interactions and driving frequency dictate translation speed. We reveal that particles moving on tissue exhibit restricted movement based on trajectory and tissue fiber orientation. Finally, we discuss that while cellular integration introduces significant adhesive drag that reduces translation speeds, it simultaneously offers a unique clinical advantage. This study highlights the potential of balancing magnetic driving parameters against biological environments to optimize for various treatment timelines and efficiency across diverse biomedical applications.

bioengineering↗

Hybrid Drosophila genomes rapidly purge minority ancestry but repeatedly retain selected regions

Hybridization is increasingly recognized as a widespread evolutionary process across animals, plants, and fungi, and plays a key role in driving speciation, shaping genetic diversity, and facilitating adaptation. Initial hybrid genomes are rarely observed empirically, making it challenging to observe in real time how competing forces like purifying selection and adaptive introgression interact to shape post-hybridization genomes. Here, we use replicated experimental hybrid populations between Drosophila simulans and D. sechellia to track directly genome-wide evolutionary dynamics across approximately 45 generations post-hybridization. We show that hybrid populations with primarily D. simulans ancestry rapidly recover wild-type levels of fertility and fecundity, whereas populations carrying predominantly D. sechellia ancestry experience persistent fitness reductions and frequent extinction. Genome-wide ancestry trajectories show pervasive purifying selection against minority-ancestry alleles, leading to rapid regression toward majority ancestry across the genome, with stronger purging on the X chromosome than autosomes. Following the initial purging, neutral minority ancestry stabilized at low frequencies across the genome. In striking contrast, we observe repeated increases in D. sechellia ancestry on chromosome 4 and multiple regions on chromosome 3R within D. simulans-majority populations, providing evidence for adaptive introgression. High-density sequencing revealed that these regions were repeatedly retained across independently evolving populations despite near-complete genome-wide purging. Simulations support a model in which recombination rapidly uncouples beneficial introgressed alleles from linked incompatibility-associated alleles during the initial generations, allowing positive selection to act. Our temporal allele-frequency analyses suggest that hybrid genome stabilization of the introgressed regions is highly repeatable but not identical, yielding parallel outcomes across replicate populations. We establish a tractable experimental framework to directly observe how hybrid genomes reorganize in real time, and demonstrate how purifying selection, positive selection, recombination, and stochastic processes interact to restructure hybrid genomes shortly after admixture.

genetics↗

Cholinergic activation of HLH-30/TFEB promotes C. elegans infection resilience.

Innate host defense depends on transcriptional programs, which support survival through two strategies that can vary independently. Resistance lowers pathogen burden, while resilience limits the damage a given burden causes. In Caenorhabditis elegans infected with Staphylococcus aureus, the highly conserved transcription factor HLH-30/TFEB drives most of the host response, which mediates infection resilience. We previously showed that EGL-30/Gq, PLC-1/PLC{varepsilon}, and DKF-1/PRKD activate HLH-30/TFEB during infection. The same phospholipase C and protein kinase D step activates TFEB in mouse macrophages infected with Salmonella or S. aureus. However, the input that drives the EGL-30/Gq, PLC-1/PLC{varepsilon}, and DKF-1/PRKD module to activate HLH-30/TFEB during infection remained unknown. Here we report that acetylcholine, acting on muscarinic receptors, is one such input. Atropine and scopolamine, two muscarinic antagonists in clinical use, as well as muscarinic receptor gene silencing blunted HLH-30/TFEB activation by infection. Moreover, a mutation of unc-17/SLC18A3 that lowers acetylcholine release from neurons impaired HLH-30/TFEB activation and induction of its target genes, while pathogen burden remained high. In uninfected animals, muscarinic agonist arecoline was sufficient to activate HLH-30/TFEB, in a muscarinic receptor-dependent manner. Nicotine, in contrast, had no effect. The agonist also lengthened survival of infection without lowering pathogen burden, in an HLH-30/TFEB-dependent manner. Silencing egl-30/GNAQ, plc-1/PLCE1, or dkf-1/PRKD1-3 cut activation by the agonist just as it cut activation by infection, showing that both stimuli require the same module. In mammals the link documented so far between acetylcholine and TFEB runs through nicotinic receptors, so whether the muscarinic route is conserved remains open. Thus, we favor a model in which infection drives neurons to release acetylcholine onto the intestinal epithelium, where muscarinic receptors acting through EGL-30/Gq, PLC-1/PLC{varepsilon}, and DKF-1/PRKD activate HLH-30/TFEB and strengthen infection resilience.

immunology↗

The south Congo Basin was critical to Bantu settlement of south central Africa

South central Africa, between the Congo Basin, the Great Lakes, and southern Africa, has long served as a corridor for human movement. Yet, it remains unclear whether there is genetic continuity between pre-Iron Age foragers and later Bantu-associated populations and whether the settlement of this region reflects multiple Bantu-associated migrations rather than the simpler serial founder model suggested by existing genomic data. To do so, we generated genome-wide ancient DNA from 71 Iron Age and historical individuals from present-day Zambia and Malawi, and analyzed these genomes alongside published data from present-day Africans. One late Iron Age individual (16th-17th century) from Kalala Island in the Kafue River, Zambia, carries 40% non Bantu related ancestry that closely matches local Later Stone Age foragers. Admixture for this individual is estimated to be 850 years ago, several centuries earlier than reported for present day BaTwa from the same region. Focusing on the Bantu-related ancestry, haplotype-based analyses identify two main clusters among Iron Age, historical, and present-day south central Bantu groups associated with different Bantu-related migrations. These results reveal a layered history in which at least two Bantu expansions radiated from the southern Congo Basin, with south central Africa acting both as a crossroads of these movements and as a staging area for the subsequent southward expansion toward southern Africa.

evolutionary biology↗

The Pan-European Impact of the Balkan Hunter-Gatherers

During the Last Glacial Maximum (LGM) 26-19 thousand years ago (kya), Europe had three principal refugia not covered by ice: the Iberian, Italian, and Balkan peninsulas1,2. While the Iberian and Italian refugia have been studied with ancient DNA3-7, the legacy of the Balkan refugium has remained a mystery due to a lack of genetic data 30-12 kya. We present genome-wide data from nine newly reported individuals: three Epipaleolithic from Romania, one Epipaleolithic from Bosnia and Herzegovina, three Mesolithic from Greece, one Epipaleolithic from Southern Italy, and one Mesolithic from Sardinia. We find that the Epipaleolithic individuals from Romania and the Mesolithic individual from mainland Greece were from a previously unsampled population that was the primary source for later European hunter-gatherers. Westward expansion of Balkan Epipaleolithic people into the Italian Peninsula and mixture with a minority contribution from pre-LGM Italians, produced a population that then spread further west to become the primary ancestry of west-ern European Mesolithic people. Northeastward expansion, bypassing Italy, contributed the European ancestry source of Scandinavian and Eastern European hunter-gatherers. Southeastward expansion to the Aegean led to Anatolian-European mixtures before the spread of farming.

genetics↗

Buried in two places: Lineages from elite Maya tombs also found in distant caves

Classic Maya societies (250-900 CE) carved out urban centers in the rainforest reaching population heights and political complexity previously unknown in the Mesoamerican tropics. Kinship was a central feature of the social fabric, and rulership was legitimized through claims of direct descent from mythical ancestors. Mortuary practices kept the dead close to the living, and ancestor veneration sometimes produced complex deposits of disarticulated remains that are difficult to identify and whose biological relationships to one another cannot be understood without genetic data. We screened 487 human tooth and bone samples and successfully generated genome-wide data for 430 of them. Of these, 341 samples representing 107 distinct individuals were recovered from both elite and non-elite tombs in a Classic period kingdom (250-900) CE in the rugged Maya Mountains of Belize. Remarkably, 24 of these individuals have skeletal elements in both an elite tomb and in a ritual tooth cache in a distant cave located 26.5km away on the other side of the Maya Mountains. These results indicate that elite lineages created ancestors from their deceased relatives in geographically expansive ways and highlights the importance of caves in the belief system of Classic Maya elites.

genetics↗

First Lithic Age Caribbean genomes document pre-Ceramic genetic continuity and affinities to Central America and northern South America

The population history of the Caribbeans first inhabitants has been challenging to reconstruct because few human remains are known from the regions earliest occupation which began around 6,000 years ago in Hispaniola, Cuba, and Puerto Rico. We generated genome-wide data from 19 individuals from Hispaniolas Samana Peninsula and focused on four who lived during the earliest pre-Ceramic "Lithic Age". Extending the Caribbean genetic record by more than a millennium to [~]4,400 calBP, we show that pre-Ceramic Age populations across Hispaniola and Cuba derive from a single ancestry source and document long-term genetic continuity across islands, with some local genetic structure within Hispaniola. Pre-Ceramic Age Caribbean ancestry shares most drift with populations from Central America and northern South America, although no sampled mainland group provides an adequate proxy. We infer very small effective community sizes, consistent with locally structured mating pools and little evidence of close-kin mating. These findings extend our understanding of Caribbean population history into its earliest phase. TeaserEarly Caribbean people shared ancestry across islands and lived in small, locally structured communities.

genetics↗

Preservation of Human Colonic Stem Cells Requires an ERK Dynamics Checkpoint Mediated by AKT

Colonic stem cells reside in a microenvironment enriched in epidermal growth factor, which is essential for their survival and can activate both PI3K-AKT and MAPK-ERK pathways. This predicts co-activation of both pathways within the growth factor-high stem cell compartment at the base of crypts. However, in patient-derived human colonic organoids and normal human tissue, stem cells maintain robust AKT activity while suppressing ERK signaling despite active EGFR engagement. As stem cells differentiate, they activate pulsatile ERK signaling, which is essential for migration, survival, and maintenance of barrier function. We show that AKT-dependent phosphorylation of RAF-1 at serine 259 establishes a post-receptor checkpoint that maintains ERK temporal dynamics in stem cells. Acute activation of ERK in stem cells triggers rapid global differentiation. Disruption of the ERK checkpoint via mutation of serine 259 leads to sustained AKT and ERK co-activation in stem cells. Unlike ERK/AKT coactivation driven by apoptosis, co-activation in the stem cell compartment results in the emergence of a neoplastic, architecturally disorganized cell population dominating the cell fate profile. Incredibly, introducing brief ERK pulses through AKT inhibition or ERK activation triggers re-differentiation of neoplastic cells. Consistent with duration-dependent MAPK encoding principles, these data demonstrate that regardless of baseline signaling amplitude, ERK signaling dynamics are epistatic to total kinase signaling load in human colonic stem cells. SIGNIFICANCEStem cells must balance self-renewal and differentiation while remaining responsive to continuous mitogenic stimulation to preserve tissue homeostasis. When self-renewal is impaired, wound healing and barrier integrity decline, whereas loss of proper differentiation drives tumorigenesis. Our findings demonstrate that this balance in the human colon is achieved through temporal control of kinase signaling rather than modulation of ligand availability. By establishing an AKT-dependent ERK dynamics checkpoint, colonic stem cells suppress differentiation-inducing ERK pulses while maintaining growth factor responsiveness. These results identify kinase dynamics as a fundamental determinant of epithelial homeostasis and suggest that subtle alterations in these dynamics may destabilize tissue organization during regeneration or chronic inflammation. Temporal encoding of kinase activity thus represents a central organizing principle in human stem cell biology.

cell biology↗

Convergent natural selection at both ends of Eurasia during parallel radical lifestyle shifts in the last ten millennia

Ancient DNA-based studies of natural selection have focused on West Eurasia due to the availability of large sample sizes, but rich insights are expected to come from comparative studies that can reveal which patterns are shared and which region-specific. We test around seven million variants for selection in 1,862 ancient East Eurasians (867 with new data) distributed over the last ten millennia. Using a generalized linear mixed model to control for population structure, we identify 40 genome-wide significant signals of selection, which have a particularly strong impact on immune and cardiometabolic traits just as in West Eurasia. East and West Eurasia show highly correlated signals of adaptation both for individual alleles and for complex traits, showing how these geographically separate groups experienced convergent evolution in response to parallel transitions to food producing economies and the accompanying lifestyle changes. An exception is the genetic determinants of light skin color: West Eurasians depigmented in the last 10,000 years, but most skin lightening in East Asians arose prior to the Holocene.

evolutionary biology↗

Subsistence transition preceded population turnover in the eastern Colombian Andes

Northwest South America was a pivotal region for human dispersals and cultural exchange during the Holocene. The Altiplano Cundiboyacense, a high-altitude plateau in the Eastern Cordillera of the Northern Andes of Colombia, preserves one of the most continuous archaeological sequences in the Americas, spanning from late Pleistocene hunter-gatherer groups to final late Holocene Muisca chiefdoms. Increasing the regional ancient DNA sample size 11-fold, we report genome-wide data from 209 individuals who lived over a period of more than 7000 years. This includes hunter-gatherers from the early-middle (10,000-7000 BP) and middle (7000-4000 BP) Holocene, initial late Holocene people (4000-2500 BP) who have the first isotopic evidence of C-enriched diets (attributed to maize), and populations associated with increasing sedentism and food production in the Herrera (2200-1300 BP) and Muisca (1200-500 BP) Periods. Previous work identified a major population turnover distinguishing earlier groups from Herrera-Muisca Period populations, but the absence of individuals dating 6000-2000 BP in that study left unresolved whether this ancestry shift was gradual or abrupt and whether it accompanied the earliest isotopic evidence of dietary input from maize or coincided with the later emergence of Herrera culture. We show that individuals predating the Herrera Period form a lineage that persisted for over five millennia, with population structure driven by drift in small groups and no detectable external gene flow. Two individuals who lived [~]2800 years ago - one directly dated to 983-835 calBCE - exhibit genetic profiles entirely consistent with hunter-gatherer ancestry yet have isotopic values consistent with the incorporation of maize into their diets, indicating subsistence change without population replacement. The emergence of Herrera culture [~]2200 BP coincided with a sharp genetic break, reflecting the migration of people carrying ancestry diverged by up to ten millennia into the Sabana de Bogota and displacing previously established peoples. By co-analyzing ancient data with modern Native Americans, we show these later populations derived from a mixture [~]4000 years ago of groups related to Chibchan language speakers of lower Central America and ones related to present-day people at the Amazonian-Andean interface who may have lived along the Chibchan expansion route. In the Herrera and Muisca Periods, genetic substructure distinguishes people from the southern and northern Altiplano, consistent with the cultural differentiation of these regions in the archaeological record. IN BRIEFAncient DNA data from the eastern Colombian Andes reveal five millennia of population continuity during which C plants were incorporated into subsistence systems without population replacement, followed later by a major ancestry turnover involving a population with ancestry admixed between that found in Chibchan-related groups and at the Amazonian-Andean interface.

genetics↗

Distinct Molecular Mechanisms Regulate Feeding State-Dependent CO2 Chemotaxis Plasticity During Different Life Stages in Caenorhabditis elegans

Across developmental stages, animals modulate their behavioural responses to external cues according to intrinsic physiological states. During development, particularly in juvenile stages, nervous systems undergo extensive changes at multiple levels. However, it remains unclear whether nervous systems at different developmental stages employ the same underlying molecular mechanisms to produce equivalent behavioural modulations in response to intrinsic or extrinsic cues. Using the model organism Caenorhabditis elegans, we identify here that animals employ distinct molecular mechanisms to achieve equivalent modulation of CO2-chemosensory behaviour at different developmental stages. Ubiquitin-proteasome-mediated downregulation of the insulin/IGF receptor, DAF-2 by the conserved quality-control ubiquitin ligase CHN-1/CHIP promotes attraction to environmental CO2 during the starvation-induced L1-arrest stage. In contrast, CO2-attaction in dauer animals is independent of CHN-1/CHIP activity. Furthermore, the feeding-induced reversal of CO2-chemotaxis to avoidance during L1-arrest exit requires the insulin/IGF pathway and the conserved CRH-1/CREB1 transcription factor activity in the CO2-sensing BAG neurons. However, induction CO2-avoidance during dauer exit is independent of CRH-1/CREB1 activity. These findings suggest that neural circuits at different life stages may utilize distinct, stage-specific molecular mechanisms to induce identical plasticity in chemosensory behaviour.

neuroscience↗

Ancient genomes from Ladakh reveal 2800-year-old mixture between Tibetans and South Asians

Reconstructing population history is harder in South Asia than in many other world regions due to a paucity of ancient DNA. We report genome-wide data for ten individuals from Old Lady Spider Cave, which lies 4000 meters above sea level in the Himalayan region of Ladakh, and dates to around 1500 years before present (BP). These individuals were genetically homogeneous and had an ancestry signature rare in South Asians today: admixed in roughly 50-50% proportions between a population well-proxied by present-day North Indians, and another genetically similar to ancient Tibetans. By analyzing the typical sizes of segments of DNA inherited from each of these ancestral populations, we find that mixture of these groups began at least fifty generation before the date of the individuals, that is, by around 2800 BP. TeaserDiscovery of a previously unknown population that lived 2800-1500 years ago in the Himalayan region of Ladakh.

evolutionary biology↗

Scm3 interacts with the N-terminal tail of Cse4 to regulate kinetochore assembly in budding yeast

The kinetochore is a multiprotein complex formed at the centromeres and is essential for the faithful chromosome segregation. In most of the organisms the kinetochore is assembled on a specialized centromeric nucleosome where histone H3 is replaced by a variant, named CENP-A. In budding yeast, the CENP-A homolog, Cse4 is recruited to the centromeric nucleosome through an interaction between its C-terminal domain and a specific chaperone, named Scm3. Interestingly, following Cse4 recruitment during S phase, Scm3 persists at the centromeres throughout the cell cycle. Recent in vitro studies have reported that Scm3 also interacts with N-terminal of Cse4 (N-C) that in turn facilitates a better interaction of Ame1-Okp1 (AO) of COMA subcomplex with N-C, which promotes kinetochore assembly. In this work, using genetic and biochemical assays we provide in vivo evidence of the interaction between Scm3 and N-C. Additionally, by artificially tethering Scm3, we show that their association has the potential to stabilize a missegregating chromosome with inactive centromere, perhaps by forming an active kinetochore at an ectopic site. We propose that at the centromeres, Scm3 has two jobs in tandem - Cse4 deposition and stabilization of N-C, which together culminates into proper kinetochore assembly. This work has clinical significance as both CENP-A and its chaperone are known to be upregulated in human cells under disease states which can predispose the cells to aneuploidy due to increased chances of forming ectopic kinetochores.

cell biology↗

Understanding proneural-mesenchymal transition using patient-derived glioma stem-like cell (GSC) organoids and engineered extracellular matrix

Glioblastoma multiforme (GBM) is a highly aggressive, angiogenic WHO grade IV glioma marked by rapid progression, therapeutic resistance, and poor prognosis. A defining feature of GBM is the presence of glioma stem-like cells (GSCs), which reside in specialized perivascular niches and drive tumor progression, recurrence, and therapeutic resistance. The blood-brain barrier, coupled with the complex and dynamic tumor microenvironment, poses significant challenges for both treatment and mechanistic investigation. Current in vitro GBM models inadequately recapitulate the structural and biochemical cues of the native perivascular niche due to the absence of functional vasculature and brain-mimetic extracellular matrix (ECM), limiting their physiological relevance and predictive power. To address the limitations of existing in vitro GBM models, we developed a patient-derived glioma stem cells (GSC) derived Matrigel spheroid system that transitions into organoids and enables integration into engineered microenvironments. Our model incorporates GSC organoids representing proneural and mesenchymal GBM subtypes, a synthetic engineered extracellular matrix (eECM), and endothelial cells (ECs) seeded on the matrix surface. We evaluated the expression of subtype-specific, pro-angiogenic, stemness, and differentiation markers under increasingly complex co-culture conditions. Our results show that Matrigel-derived GSC spheroids progressively differentiate into organoids over two weeks, with significantly enhanced expression of cell-specific markers in the presence of ECs. Encapsulation of these organoids within eECM, combined with EC co-culture, further promoted cellular invasion and induction of GBM associated genes. This in situ encapsulation strategy enables real-time observation of GSC behavior in a tunable microenvironment that mimics key features of the native tumor niche. Together, this platform provides a physiologically relevant and modular in vitro system for investigating GBM pathophysiology. It holds promise for uncovering tumor-specific cellular dependencies, studying GSC-vascular interactions, and conducting high-throughput drug screening under controlled, biomimetic conditions. SignificanceThis study establishes a 3D GSC organoid model with engineered matrix to investigate glioblastoma plasticity and vascular mimicry.

cancer biology↗

Hematopoietic stem cell conditioned media induces excessive mitochondrial fission via Drp-1 to target colorectal cancer

Mitochondria, often referred to as the "powerhouses of the cell," are particularly crucial in cancer cells due to their high energy demands. Mitochondrial fusion-fission dynamics play a critical role in regulating signaling pathways and metabolic activities in colorectal cancer (CRC) cells. Increased mitochondrial fission drives metabolic reprogramming, enabling CRCs to proliferate, metastasize, and resist chemotherapy. Paradoxically, excessive fission induces mitochondria-mediated apoptosis. Our previous studies have shown that hematopoietic stem cell-derived conditioned media (CM) modulate the apoptosis pathway and mitochondrial bioenergetics of cancer stem cells by altering the cancer microenvironment. In this study, We found that HSCs-CM facilitates excessive fission in colorectal cancer cells by modulating Drp-1 and concurrently activating the PINK1-Parkin mitophagy pathway and intrinsic apoptosis, leading to loss of viability of these cells. Moreover, proteomics data showed that HSCs-CM dysregulated the electron transport chain complexes, with an exceptionally high degree of dysregulation of complexes III and IV. Metabolomics revealed dysregulation of critical metabolites, RNA sequencing revealed dysregulation of transcripts, and proteomics revealed dysregulation of proteins, involved in mitochondrial bioenergetics and the autophagy pathway in CRCs treated with CM. Taken together, our studies reveal the therapeutic potential of HSC-conditioned media for treating colorectal cancer. HighlightsO_LIHematopoietic stem cell-derived conditioned media (HSC-CM) induces excessive mitochondrial fission in colorectal cancer (CRC) cells by upregulating Drp-1, thereby activating the intrinsic apoptotic pathway. C_LIO_LIExcessive fission and bioenergetic dysfunction caused by HSC-CM result in loss of mitochondrial membrane potential and elevated reactive oxygen species production. C_LIO_LIHSC-CM severely disrupts the electron transport chain in CRC cells, precipitating an energy crisis and engaging the PINK1-mediated mitophagy pathway. C_LI SummaryHematopoietic stem cell-derived conditioned media (HSC-CM) compromises mitochondrial dynamics by inducing excessive fission in colorectal cancer (CRC) cells through upregulation of Drp-1 and its associated protein complex. The resulting hyperfission leads to severe mitochondrial dysfunction, characterised by a loss of mitochondrial membrane potential, decreased ATP production, and disrupted electron transport chain complexes. This bioenergetic crisis and overproduction of reactive oxygen species ultimately trigger intrinsic apoptosis and engage the mitophagy pathway, leading to loss of CRC cell viability.

cancer biology↗

Microclimatic heterogeneity is associated with forest structural complexity and biodiversity

Forest microclimates, their dependence on forest structure, and their impact on biodiversity are crucial for future forest management under climate change. However, standard approaches for measuring forest microclimates do not capture within-plot heterogeneity, which, according to the habitat heterogeneity hypothesis, is a key driver of local biodiversity. We quantified horizontal and vertical microclimatic heterogeneity within 30 broad-leaved forest plots in Central Europe using a three-dimensional design with high spatial resolution. Moreover, we examined whether microclimatic heterogeneity differs among silvicultural treatments and whether it can be predicted using forest structure indices derived from laser scanning. Additionally, we explored the relationship between microclimatic heterogeneity and biodiversity. In the understory of canopy gaps, warm and cold habitats co-existed in close proximity, leading to a high horizontal microclimatic heterogeneity. In closed stands with high structural complexity, we found steep gradients of increasing temperature and vapor pressure deficit from the ground to the canopy during mid-day. Canopy cover and forest structural complexity were strong indicators of microclimatic heterogeneity. We found positive relationships between herb layer temperature heterogeneity and the diversity of plants, Hymenoptera, and Diptera. Our results demonstrate that single-point measurements fail to capture the substantial microclimatic heterogeneity within plots, potentially misrepresenting the conditions experienced by forest species. However, laser scanning provides reliable indicators for within- plot microclimatic heterogeneity. With canopy gaps featuring high horizontal microclimatic heterogeneity and promoting the biodiversity of several taxonomic groups, we argue that managing forests for maximized temperature buffering should not be the only strategy to conserve forest biodiversity. HighlightsO_LIHigh small-scale horizontal microclimatic heterogeneity in canopy gaps C_LIO_LISteep vertical microclimatic gradients in closed-canopy forests C_LIO_LICanopy cover and structural complexity: indicators for microclimatic heterogeneity C_LIO_LIPositive relationship between herb layer temperature heterogeneity and biodiversity C_LI

ecology↗

Higher bat and bird γ-diversity in structurally complex forests is driven by distinct α- and β-diversity responses

Effective conservation management and habitat restoration rely on understanding how biodiversity responds to environmental change. Centuries of silviculture have homogenized forests and their species communities globally, reducing biodiversity. To test whether restoring forest structural complexity can promote biodiversity, we conducted a large-scale, spatially explicit landscape experiment. At 11 sites across Germany, we compared bat and bird diversity in forests with experimentally enhanced heterogeneity by increasing deadwood and canopy complexity to homogeneous production forests. Both taxa were investigated by autonomous acoustic recorders and automatic species identification. We quantified within-patch (-), between-patch ({beta}-), and landscape-level ({gamma}-) diversity, emphasizing infrequent to highly frequent species for taxonomic, functional, and phylogenetic diversity. The pairwise comparisons of the sites were synthesized using a newly developed meta-analysis of rarefaction-extrapolation curves. {gamma}-diversity increased significantly in structurally heterogeneous forests for both taxa, albeit through distinct taxon-specific mechanisms. Bat {gamma}-diversity gains were primarily driven by higher {beta}-diversity, indicating greater dissimilarity in species assemblages among patches, while bird {gamma}-diversity increased via higher -diversity within patches. Bat diversity increases were mainly taxonomic, suggesting functional similarity in the communities, whereas birds showed the highest gains in functional diversity, indicating that experimental treatments resulted in greater trait dissimilarity. Our results provide experimental evidence under real-world conditions that {gamma}-diversity can be shaped by different diversity mechanisms. These patterns likely originate from differences in activity ranges, such as the large-scale movements of foraging bats in contrast to the more spatially restricted, territorial behavior of birds. This highlights the need for taxon-specific restoration strategies in homogenized landscapes.

ecology↗

Parasitoids reduce growth rate in oak-feeding caterpillars

O_LIKoinobiont parasitoids have been shown to both reduce and increase the growth rate of caterpillars. However, no comprehensive study has been conducted on all caterpillar hosts of a given plant species. Moreover, most of the existing case studies are on large caterpillars attacking crop plants. This may not be representative of the effect of parasitoids on caterpillar growth on trees. C_LIO_LIWe measured the growth rate of parasitised and non-parasitised spring caterpillars collected from oak trees (Quercus robur & Q. petraea) in France and Poland. C_LIO_LIAcross six species of Lepidoptera, parasitoids reduced caterpillar growth rate on average. C_LIO_LIFurther studies should determine if the reduced growth rate is accompanied by lower consumption rates, so that the plant directly benefits from attracting parasitoids when they are attacked by caterpillars. C_LI

ecology↗