Biology subjects

Matsumura, T.

Publications and source records attributed to Matsumura, T..

18 recordsLinked to original sources

bioRxiv2026

Inflammatory restraint and membrane lipid integrity protect hematopoietic stem cells under stress

Life-long production of blood requires the preservation of hematopoietic stem cell (HSCs) regenerative capacity during inflammation. The cytokine, Thrombopoietin (THPO), is essential for HSC maintenance yet its role during inflammatory stress remains incompletely understood. Long-term repopulating potential was rapidly depleted in THPO-deficient HSCs upon poly(I:C) administration through inflammatory pyroptosis. Transcriptomic and chromatin accessibility analyses revealed constitutive interferon (IFN) pathway activation in THPO-deficient HSCs, characterized by enhanced STAT1 signaling, increased accessibility of STAT and IRF motifs, and elevated expression of IFN-stimulated genes. Lipidomic profiling further identified selective shifts in sphingomyelin (SM) species and enrichment of features associated with increased bilayer rigidity. THPO-deficient HSCs displayed elevated membrane SM incorporation, impaired membrane fluidity and altered membrane ultrastructure. Genetic ablation of Stat1 normalized membrane lipid abnormalities and reduced pyroptotic activation and restored HSC survival and regenerative function under inflammatory stress. Together, these findings identify a STAT1 and SM metabolism as critical THPO downstream to protect HSCs from inflammatory pyroptosis. Our results reveal membrane lipid homeostasis as a fundamental mechanism through which cytokine signaling safeguards HSC function during stress.

cell biology↗

bioRxiv2026

LRP1 is an entry receptor for the botulinum toxin complex in the gut

Botulinum neurotoxin (BoNT) is an etiologic agent of food poisoning caused by Clostridium botulinum. The large progenitor toxin complex (L-PTC) crosses the intestinal epithelial barrier to deliver BoNT to target neurons; however, it is not clearly understood how BoNT enters the host. Here, we identified low-density lipoprotein receptor-related protein 1 (LRP1) as a major enterocyte transcytosis receptor for the hyper-oral-toxic L-PTC serotype B-Okra (L-PTC/BOkra). We found that hemagglutinin (HA), a neurotoxin-associated protein within the L-PTC/BOkra complex, binds to LRP1 via N-glycans. HA/BOkra co-localized with LRP1 within the internalized vesicles in cultured cells and enterocytes. LRP1 deletion inhibited the apical-to-basal transcytosis of L-PTC/BOkra in an intestinal epithelial cell line, and this effect was rescued by LRP1 re-expression. Finally, intestinal epithelial cell-specific LRP1-deficient mice displayed reduced susceptibility to toxicity caused by oral administration of L-PTC/BOkra. Taken together, these results indicate that N-glycosylated LRP1 mediates L-PTC/BOkra transcytosis via enterocytes, enabling BoNT to traverse the intestinal epithelial barrier.

microbiology↗

bioRxiv2026

Acquisition of Stickland-metabolizing bacteria during infancy prevents Clostridium botulinum infection

Infant botulism is caused by intestinal colonization with Clostridium botulinum, whereas healthy adults are resistant. Although the gut microbiota has long been implicated in protection against C. botulinum, its bacterial basis has remained unknown. Here, we show that specific amino acid-metabolizing bacteria confer resistance to C. botulinum colonization through nutrient competition. Longitudinally collected human infant microbiotas exhibited a transition from susceptibility to resistance after transplantation into germ-free mice. 5-Aminovalerate marked the resistant microbiota, implicating Stickland metabolism. Resistant microbiotas were enriched in Stickland-metabolizing Clostridia, including Clostridioides difficile. Metabolomics revealed overlapping amino acid utilization, and C. difficile suppressed C. botulinum expansion through amino acid competition. These findings demonstrate that acquisition of Stickland-metabolizing Clostridia during infancy prevents C. botulinum infection through competition for shared amino-acid-dependent nutritional niches.

microbiology↗

bioRxiv2026

An Antibiotic-Treated Mouse Model Reveals the Progression of Intestinal Botulism

Intestinal botulism, including infant botulism and adult intestinal toxemia botulism, is a life-threatening disease caused by intestinal infection with Clostridium botulinum (Cb) spores. Infants are particularly susceptible to Cb infection because of their immature gut microbiota, whereas healthy adults are generally protected by gut microbiota-mediated colonization resistance. Thus, immature gut microbiota or gut dysbiosis is thought to permit Cb colonization. However, the mechanisms underlying colonization resistance and disease progression remain poorly characterized. Here, using adult mice with antibiotic-induced dysbiosis, we established a model for studying Cb infection and characterized intestinal colonization, bacterial expansion, BoNT accumulation, and disease progression during intestinal botulism. Intestinal botulism developed in antibiotic-treated mice after intragastric administration of strain 62A spores, whereas untreated adult mice showed no symptoms. In antibiotic-treated mice, Cb expanded over time in fecal samples, followed by accumulation of BoNT/A, which correlated with the progression of botulism symptoms. Cb growth and BoNT/A accumulation occurred mainly in the cecum and colon, but not in the small intestine. Furthermore, this mouse model was applicable to the analysis of intestinal botulism caused by other Cb strains, including 7I03-H, Okra, and Osaka05. Taken together, this mouse model provides a useful platform for elucidating the pathogenesis of intestinal botulism and developing novel therapeutic strategies.

microbiology↗

bioRxiv2025

Gut mucin fucosylation dictates the entry of botulinum toxin complexes

Botulinum toxins (BoNTs) are the most potent known bacterial toxins. The BoNT complex from Clostridium botulinum B-Okra (large progenitor toxin complex (L-PTC)/BOkra, hyper-oral-toxic) exerts at least 80-fold higher oral toxicity1 in mice compared with that from serotype A1 (L-PTC/A62A, non-hyper-oral-toxic). Here, we showed that L-PTC/BOkra was predominantly absorbed through enterocytes, whereas L-PTC/A62A targeted intestinal microfold cells. Furthermore, we demonstrated that 1,2-fucosylation of intestinal mucin determined the oral toxicity of L-PTCs as well as their entry routes; more specifically, these routes were governed by the carbohydrate-binding spectrum of hemagglutinin (HA) complex, which is one of the L-PTC components. Disruption of fucosylation in fucosyltrasferase-2 (Fut2)-null mice hindered the intestinal mucin penetration of L-PTC/BOkra via HA and reduced the susceptibility to its oral intoxication. Our data establish the molecular mechanism by which the oral toxicity of BoNTs is increased after they cross intestinal mucus layers.

microbiology↗

bioRxiv2024

Stress-induced organismal death is genetically regulated by the mTOR-Zeste-Phae1 axis

All organisms are exposed to various stressors, which can sometimes lead to organismal death, depending on their intensity. While stress-induced organismal death has been observed in many species, the underlying mechanisms remain unclear. In this study, we investigated the molecular mechanisms of stress-induced organismal death in the fruit fly Drosophila melanogaster. We identified a chymotrypsin-like serine protease Phaedra1 (Phae1) as a death mediator in D. melanogaster larvae. Phae1 expression was upregulated by lethal heat stress (40 {degrees}C) but not non-lethal heat stress (38 {degrees}C or lower). The most prominent induction of Phae1 occurred in the central nervous system (CNS). We found neuro-specific knockdown of Phae1 increased survival and reduced neuronal caspase activity following exposure to lethal heat stress, suggesting that the transcriptional upregulation of Phae1 in the CNS is essential for stress-induced organismal death. We next found via bioinformatic and biochemical analyses that the transcription factor Zeste (Z) bound the Phae1 enhancer region and that z loss-of-function impaired Phae1 induction in the CNS, increasing survival following lethal heat stress. In addition, we found via chemical screening that rapamycin, a chemical inhibitor of mechanistic target of rapamycin (mTOR), suppressed Phae1 expression. Neuro-specific knockdown of mTor reduced the protein levels of both Phae1 and Z, leading to an increase in survival following lethal heat stress. Together, these results indicate that heat stress-induced organismal death in D. melanogaster larvae is regulated by a genetically encoded transcriptional signaling pathway involving the mTOR-Z-Phae1 axis.

physiology↗

bioRxiv2024

A microendovascular system can record precise neural signals from cortical and deep vessels with minimal invasiveness

Minimally invasive intravascular electroencephalography (ivEEG) signals are a promising tool for developing clinically feasible brain-computer interfaces (BCIs) that restore communication and motor functions in paralyzed patients. However, current ivEEG techniques can only record signals from the superior sagittal sinus (SSS), making it challenging to record motor responses related to hand and mouth movements from brain regions distant from the SSS, despite their critical role in BCIs. Here, using micro intravascular electrodes, ivEEGs recorded from the cortical or deep veins of eight pigs could measure cortical activities with greater signal power and better spatial resolution than those recording in the SSS, thus allowing mapping of the sensorimotor and visual functional areas. Additionally, electrical stimulation in the cortical vein between the micro intravascular electrodes induced muscle contractions contralateral to the stimulated area in five anesthetized pigs. These results demonstrate that ivEEG using micro intravascular electrodes is a promising tool for developing BCIs.

neuroscience↗

bioRxiv2022

Analysis of splicing abnormalities in the white matter of myotonic dystrophy type 1 brain using RNA-sequence

Myotonic dystrophy type 1 (DM1) is a neuromuscular disorder caused by the genomic expansions of CTG repeats, in which RNA-binding proteins, such as muscleblind-like protein, are sequestered in the nucleus, and abnormal splicing is observed in various genes. Although abnormal splicing reportedly occurs in the brains of patients with DM1, it is relation to the central nervous system symptoms is unknown. Several imaging studies have indicated substantial white matter (WM) defects in patients with DM1. Here, we performed RNA-sequencing and analysis of CTG repeat lengths in the frontal lobe of patients with DM1, separating the grey matter (GM) and WM, to investigate the splicing abnormalities in the DM1 brain, especially in the WM. The results demonstrated the number of repeats in the GM tended to be increase, with several genes showing similar levels of splicing abnormalities in the GM and WM, suggesting that the WM defects in DM1 are not only caused by aberrant splicing of GM RNA but also of WM RNA, which could be attributed to abnormal splicing of glial cell RNAs.

molecular biology↗

bioRxiv2022

DHCR7 as a novel regulator of ferroptosis in hepatocytes

Recent evidence indicates that ferroptosis is implicated in the pathophysiology of various liver diseases; however, the mechanism of ferroptosis regulation in the liver is poorly understood. Here, using the whole-genome screening approach, we identified 7-dehydrocholesterol reductase (DHCR7), the terminal enzyme of cholesterol biosynthesis, as a novel regulator of ferroptosis in hepatocytes. Genetic and pharmacological inhibition (with AY9944) of DHCR7 suppressed lipid peroxidation and ferroptosis in human hepatocellular carcinoma Huh-7 cells. DHCR7 inhibition increased its substrate, 7-dehydrocholesterol (7-DHC), and extrinsic 7-DHC supplementation in turn suppressed ferroptosis. On the other hand, cholesterol deprivation had no effect on ferroptosis. A 7-DHC-derived oxysterol metabolite, 3{beta},5-dihydroxycholest-7-en-6-one (DHCEO), was increased by a ferroptosis inducer RSL-3 in DHCR7-deficient cells, suggesting that the ferroptosis-suppressive effect of DHCR7 inhibition was driven by intracellular 7-DHC as a radical scavenger. While extrinsic 7-DHC supplementation suppressed ferroptosis in various cancer cells, pharmacological DHCR7 inhibition by AY9944 showed cell-type specific effects, which could be explained by high DHCR7 expression in Huh-7 cells. We further showed that AY9944 suppressed ferroptosis in murine primary hepatocytes in vitro and systemic administration of AY9944 inhibited hepatic ischemia-reperfusion injury in vivo. These findings provide new insights into the regulatory mechanism of liver ferroptosis and suggest that DHCR7 inhibition is a potential therapeutic option for ferroptosis-related liver diseases.

molecular biology↗

bioRxiv2021

Two doses of mRNA vaccine elicit cross-neutralizing memory B-cells against SARS-CoV-2 Omicron variant

SARS-CoV-2 Beta and Omicron variants have multiple mutations in the receptor-binding domain (RBD) allowing antibody evasion. Despite the resistance to circulating antibodies in those who received two doses of mRNA vaccine, the third dose prominently recalls cross-neutralizing antibodies with expanded breadth to these variants. Herein, we longitudinally profiled the cellular composition of persistent memory B-cell subsets and their antibody reactivity against these variants following the second vaccine dose. The vaccination elicited a memory B-cell subset with resting phenotype that dominated the other subsets at 4.9 months. Notably, most of the resting memory subset retained the ability to bind the Beta variant, and the memory-derived antibodies cross-neutralized the Beta and Omicron variants at frequencies of 59% and 29%, respectively. The preservation of cross-neutralizing antibody repertoires in the durable memory B-cell subset likely contributes to the prominent recall of cross-neutralizing antibodies following the third dose of the vaccine. One Sentence SummaryFully vaccinated individuals preserve cross-neutralizing memory B-cells against the SARS-CoV-2 Omicron variant.

immunology↗

bioRxiv2021

Depth-targeted intracortical microstroke by two-photon photothrombosis in rodent brain

SignificancePhotothrombosis is a widely used model of ischemic stroke in rodent experiments. In the photothromboris model, the photosensitizer Rose Bengal is systemically introduced to the blood stream and activated by green light to induce aggregation of platelets that eventually cause vessel occlusion. Since the activation of Rose Bengal is a one-photon phenomenon and the molecules in the illuminated area (light path) are subject to excitation, targeting of thrombosis is unspecific especially in the depth dimension. We have developed a photothrombosis protocol that can target a single vessel in the cortical parenchyma by two-photon excitation. AimWe aim to induce a thrombotic stroke in the cortical parenchyma by two-photon activation of Rose Bengal so that we confine photothrombosis within a vessel of a target depth. ApproachFITC-dextran is injected into the blood stream to visualize the cerebral blood flow in anesthetized adult mice with a cranial window. After a target vessel is chosen by two-photon imaging (950 nm), Rose Bengal is injected into the blood stream. The scanning wavelength is changed to 720 nm and photothrombosis was induced by scanning the target vessel. ResultsTwo-photon depth-targeted single vessel photothrombosis was achieved with a success rate of 84.9{+/-}1.7% within 80 s. Attempts without Rose Bengal (i.e., only with FITC) did not result in photothrombosis at the excitation wavelength of 720 nm. ConclusionsWe described a protocol that achieves depth-targeted single vessel photothrombosis by two-photon excitation. Simultaneous imaging of blood flow in the targeted vessel using FITC dextran enabled the confirmation of vessel occlusion and prevention of excess irradiation that possibly induces unintended photodamage.

neuroscience↗

bioRxiv2021

Cryo-sensitive aggregation triggers NLRP3 inflammasome assemblyin cryopyrin-associated periodic syndrome

Cryopyrin-associated periodic syndrome (CAPS) is an autoinflammatory syndrome caused by mutations of NLRP3, which was originally identified as cryopyrin. Familial cold autoinflammatory syndrome (FCAS), the mildest form of CAPS, is characterized by cold-induced inflammation induced by the overproduction of IL-1{beta}. However, the molecular mechanism of how mutated NLRP3 causes inflammasome activation in CAPS remains unclear. Here, we found that CAPS-associated NLRP3 mutants form cryo-sensitive aggregates that function as a scaffold for inflammasome activation. Cold exposure promoted inflammasome assembly and subsequent IL-1{beta} release triggered by mutated NLRP3. While K+ efflux was dispensable, Ca2+ was indispensable for mutated NLRP3-mediated inflammasome assembly. Notably, Ca2+ influx was induced during mutated NLRP3-mediated inflammasome assembly. Furthermore, caspase-1 inhibition prevented Ca2+ influx and inflammasome assembly induced by the mutated NLRP3, suggesting a feed-forward Ca2+ influx loop triggered by mutated NLRP3. Thus, the mutated NLRP3 forms cryo-sensitive aggregates to promote inflammasome assembly distinct from canonical NLRP3 inflammasome activation.

immunology↗

bioRxiv2021

Identification, crystallization and epitope determination of public TCR shared and expanded in COVID-19 patients

T cells play pivotal roles in protective immunity against SARS-CoV-2 infection. Follicular helper T (Tfh) cells mediate the production of antigen-specific antibodies; however, T cell receptor (TCR) clonotypes used by SARS-CoV-2-specific Tfh cells have not been well characterized. Here, we first identified and crystallized public TCR of Tfh clonotypes that are shared and expanded in unhospitalized COVID-19-recovered patients. These clonotypes preferentially recognized SARS-CoV-2 spike (S) protein epitopes which are conserved among emerging SARS-CoV-2 variants. These clonotypes did not react with S proteins derived from common cold human coronaviruses, but cross-reacted with symbiotic bacteria, which might confer the publicity. Among SARS-CoV-2 S epitopes, S864-882, presented by frequent HLA-DR alleles, could activate multiple public Tfh clonotypes in COVID-19-recovered patients. Furthermore, S864-882-loaded HLA tetramer preferentially bound to CD4+ T cells expressing CXCR5. In this study, we identified and crystallized public TCR for SARS-CoV-2 that may contribute to the prevention of COVID-19 aggravation.

immunology↗

bioRxiv2020

Synthesis and preclinical evaluation of MTP38 as a novel PET ligand for phophodiesterase 7 in the brain

PurposePhosphodiesterase (PDE) 7 is a potential therapeutic target for neurological and inflammatory diseases, although in-vivo visualization of PDE7 has not been successful. In this study, we aimed to develop [11C]MTP38 as a novel positron emission tomography (PET) ligand for PDE7. Methods[11C]MTP38 was radiosynthesized by 11C-cyanation of a bromo precursor with [11C]HCN. PET scans of rat and rhesus monkey brains and in-vitro autoradiography of brain sections derived from these species were conducted with [11C]MTP38. In monkeys, dynamic PET data were analyzed with an arterial input function to calculate the total distribution volume (VT). The non-displaceable binding potential (BPND) in the striatum was also determined by a reference tissue model with cerebellar reference. Finally, striatal occupancy of PDE7 by an inhibitor was calculated in monkeys according to changes in BPND. Results[11C]MTP38 was synthesized with radiochemical purity [≥] 99.4% and molar activity of 38.6 {+/-} 12.6 GBq/mol. Autoradiography revealed high radioactivity in the striatum and its reduction by non-radiolabeled ligands, in contrast with unaltered autoradiographic signals in other regions. In-vivo PET after radioligand injection to rats and monkeys demonstrated that radioactivity was rapidly distributed to the brain and intensely accumulated in the striatum relative to the cerebellum. Correspondingly, estimated VT values in the monkey striatum and cerebellum were 3.59 and 2.69 mL/cm3, respectively. The cerebellar VT value was unchanged by pretreatment with unlabeled MTP38. Striatal BPND was reduced in a dose-dependent manner after pretreatment with MTP-X, a PDE7 inhibitor. Relationships between PDE7 occupancy by MTP-X and plasma MTP-X concentration could be described by Hills sigmoidal function. ConclusionWe have provided the first successful preclinical demonstration of in-vivo PDE7 imaging with a specific PET radioligand. [11C]MTP38 is a feasible radioligand for evaluating PDE7 in the brain and is currently being applied to a first-in-human PET study.

neuroscience↗

bioRxiv2020

The Drosophila Individual Activity Monitoring and Detection System (DIAMonDS)

Here, we have developed DIAMonDS (Drosophila Individual Activity Monitoring and Detection System) comprising time-lapse imaging by a charge-coupled device (CCD) flatbed scanner and Sapphire, a novel algorithm and web application. DIAMonDS automatically and sequentially identified the transition time points of multiple life cycle events such as pupariation, eclosion, and death in individual flies at high temporal resolution and on a large scale. DIAMonDS performed simultaneous multiple scans to measure individual deaths ([≤] 1,152 flies per scanner) and pupariation and eclosion timings ([≤] 288 flies per scanner) under various chemical exposures, environmental conditions, and genetic backgrounds. DIAMonDS correctly identified 74-85% of the pupariation and eclosion events and [~]92% of the death events within {+/-}10 scanning frames. This system is a powerful tool for studying the influences of genetic and environmental factors on fruit flies and efficient, high-throughput genetic and chemical screening in drug discovery.

developmental biology↗

bioRxiv2019

Fully Human Monoclonal Antibodies Effectively Neutralizing Botulinum Neurotoxin Serotype B

Botulinum neurotoxin (BoNT) is the most potent natural toxin known. Of the seven BoNT serotypes (A to G), types A, B, E, and F cause human botulism. Treatment of human botulism requires the development of effective toxin-neutralizing antibodies without side effects such as serum sickness and anaphylaxis. In this study, we generated fully human monoclonal antibodies (HuMAbs) against serotype B BoNT (BoNT/B1) using a murine-human chimera fusion partner cell line named SPYMEG. Of these HuMAbs, M2, which specifically binds to the light chain of BoNT/B1, showed neutralization activity in a mouse bioassay (approximately [≥] 100 i.p. LD50/mg of antibody), and M4, which binds to the C-terminal of heavy chain, showed partial protection. The combination of M2 and M4 was able to completely neutralize BoNT/B1 with a potency greater than 10,000 i.p. LD50/mg of antibodies, and was effective both prophylactically and therapeutically in the mouse model of botulism. Moreover, this combination showed broad neutralization activity against three type B subtypes, namely BoNT/B1, BoNT/B2, and BoNT/B6. These data demonstrate that the combination of M2 and M4 is promising in terms of a foundation for new human therapeutics for BoNT/B intoxication. IMPORTANCEBotulinum neurotoxins (BoNTs) produced by Clostridium botulinum and related species cause human botulism. Immunotherapy is the most effective treatment for botulism and equine immune serum formulations are used in cases of human botulism. However, these antisera may cause serum sickness or anaphylaxis. Additionally, the production of immune sera involves complicated and time-consuming manufacturing processes and quality management. Therefore, the development of safe, effective, and higher productive antibodies is required. Here we generated fully human monoclonal antibodies against serotype B BoNT (BoNT/B). We found that the combination of these antibodies (M2+M4) had potent and broad neutralization activity against BoNT/B, and showed therapeutic and preventive effects against botulism in mouse models. These data indicate that M2+M4 are promising candidates for the development of human therapeutics and prophylactics for BoNT/B intoxication.

microbiology↗

bioRxiv2019

Differences in splicing defects between the grey and white matter in myotonic dystrophy type 1

Myotonic dystrophy type 1 (DM1) is a multi-system disorder caused by CTG repeats in the myotonic dystrophy protein kinase (DMPK) gene. This leads to sequestration of the splicing factor, muscleblind-like 2 (MBNL2), and aberrant splicing, mainly in the central nervous system. We investigated the splicing patterns of MBNL1/2 and genes controlled by MBNL2 in several regions of the brain and between the grey matter (GM) and white matter (WM) in DM1 patients using RT-PCR. Compared with the control, the percentage of spliced-in parameter (PSI) for most of the examined exons were significantly altered in most of the brain regions of DM1 patients, except for the cerebellum. The splicing of many genes was differently regulated between the GM and WM in both DM1 and control. The level of change in PSI between DM1 and control was higher in the GM than in the WM. The differences in alternative splicing between the GM and WM may be related to the effect of DM1 on the WM of the brain. We hypothesize that in DM1, aberrantly spliced isoforms in the neuronal cell body of the GM may not be transported to the axon. This might affect the WM as a consequence of Wallerian degeneration secondary to cell body damage. Our findings may have implications for analysis of the pathological mechanisms and exploring potential therapeutic targets.

molecular biology↗

bioRxiv2019

Repeated phenotypic selection for cuticular blackness of armyworm larvae decreased stress resistance

Armyworm Mythimna separata larvae show changes in cuticle darkening depending on population densities and are roughly categorized into two phenotypes, a pale brown solitary type and black-colored gregarious type. Although the color difference in both larval types is apparent, it remains ambiguous whether any change in physiological traits accompanies the cuticle darkening. To answer this query, we repeated genetic selection of the blackness phenotype over one hundred generations in our laboratory colony and produced a black-colored (BL) strain. Comparison between non-selected control (CTL) and BL strains revealed an increased fecundity and adult life span in the BL strain compared with the CTL strain. In contrast, BL strain larvae were found to be significantly more sensitive to heat stress than CTL strain larvae. Hemolymph reactive oxygen species (ROS) levels were higher in the BL strain than in the CTL strain irrespective of stress. Antioxidant activities of the hemolymph were not significantly different between the two strains under non-stress condition, but the activities increased to higher levels in the CTL strain than those in the BL strain after heat stress. Activities and gene expression levels of antioxidant enzymes such as catalase and superoxide dismutase (SOD) in the fat body were significantly higher in CTL strain larvae than in BL strain larvae after heat treatment. Analysis of heat stress tolerance of F1 hybrids of CTL and BL strain adults showed that phenotype of stress tolerance was inherited maternally. These results indicate a trade-off between reproductive activity and stress resistance during repeated genetic selection.\n\nSummary statementDiscrete cuticle color change from whitish to blackish, which was created by repeating the reciprocal crossing of selected dark-colored individuals, increased fecundity but lowered stress tolerance in the armyworm.

physiology↗