1.1 109 info:srw/schema/1/mods-v3.3xml journalArticle published yes 15 S. Meyer author E. M. Caldarone author M. A. Chicharo author C. Clemmesen author A. M. Faria author C. Faulk author A. Folkvord author G. J. Holt author H. Hoie author P. Kanstinger author A. Malzahn author Damian Moran author 7a0e6f39-191d-45f7-9231-60b7f3984049 C. Petereit author J. G. Stottrup author M. A. Peck author Functional zoology v1000610 department Gaining reliable estimates of how long fish early life stages can survive without feeding and how starvation rate and time until death are influenced by body size, temperature and species is critical to understanding processes controlling mortality in the sea. The present study is an across-species analysis of starvation-induced changes in biochemical condition in early life stages of nine marine and freshwater fishes. Data were compiled on changes in body size (dry weight, DW) and biochemical condition (standardized RNA-DNA ratio, sRD) throughout the course of starvation of yolk-sac and feeding larvae and juveniles in the laboratory. In all cases, the mean biochemical condition of groups decreased exponentially with starvation time, regardless of initial condition and endogenous yolk reserves. A starvation rate for individuals was estimated from discrete 75th percentiles of sampled populations versus time (degree-days, Dd). The 10th percentile of sRD successfully approximated the lowest, life-stage-specific biochemical condition (the edge of death). Temperature could explain 59% of the variability in time to death whereas DW had no effect. Species and life-stage-specific differences in starvation parameters suggest selective adaptation to food deprivation. Previously published, interspecific functions predicting the relationship between growth rate and sRD in feeding fish larvae do not apply to individuals experiencing prolonged food deprivation. Starvation rate, edge of death, and time to death are viable proxies for the physiological processes under food deprivation of individual fish pre-recruits in the laboratory and provide useful metrics for research on the role of starvation in the sea. (C) 2011 Elsevier B.V. All rights reserved. https://portal.research.lu.se/en/publications/8e80186c-2d6a-40b8-bce5-394182c6fdd7 Elsevier 2012 eng RNA-DNA ratio Starvation rate Mortality threshold Time to death Percentile approach Zoology 0924-7963 2516931 000300591800003 84455205710 10.1016/j.jmarsys.2011.09.010 http://dx.doi.org/10.1016/j.jmarsys.2011.09.010 yes 93 11 24 https://www.scopus.com/pages/publications/84455205710 8e80186c-2d6a-40b8-bce5-394182c6fdd7 2016-04-01T12:52:30+02:00 2025-10-14T12:49:06+02:00 2016-04-01T12:52:30+02:00 1 info:srw/schema/1/mods-v3.3xml journalArticle published yes 4 Martina Holst author 285f31fc-2454-4393-9c42-a110791479b2 Benjamin Frydman author Laurance J. Marton author Stina Oredsson author a8f39329-4536-42b1-a5b9-e93a9df7f3eb Functional zoology v1000610 department Polyamine analogues have demonstrated anti-tumour activity in a number of solid tumour models. In the present study we<br/><br> compared the cytotoxicities of three polyamine analogues against four breast cancer cell lines. All cell lines are derived from tumours of women with breast cancer and, although we are sampling just a small number of tumours, they represent a spectrum of the genetic plethora of breast cancers. Cytotoxicity, over a dose range from 0.1 to 100 microM, was evaluated with three different<br/><br> cytotoxicity assays performed in 96-well plates. Comparing the effects of the analogues on polyamine pools with data from the cytotoxicity assays indicates that there was not a direct correlation between polyamine pool depletion and cytotoxicity. Flow cytometry was used to investigate analogue-induced cell death as measured by the appearance of a sub-G1 peak. Induction of cell death by the analogues differed in the cell lines, however, cell death when induced was apoptotic, as demonstrated by detection of<br/><br> apoptotic bodies with immunofluorescence microscopy of propidium iodide-stained nuclei. Comparing the flow cytometry-derived data and the data from the cytotoxicity assays reveals that the analogues exert their effects by inhibiting cell growth and/or inducing cell death. https://portal.research.lu.se/en/publications/961892b0-e557-486f-939a-364e77258271 Elsevier 2006 eng Polyamine analogues Human breast cancer CGC-11158 CGC-11047 CGC-11093 Cell death Zoology 0300-483X 168008 000238346300009 16697514 33646597294 10.1016/j.tox.2006.03.009 http://dx.doi.org/10.1016/j.tox.2006.03.009 yes 223 1-2 71 81 https://www.scopus.com/pages/publications/33646597294 961892b0-e557-486f-939a-364e77258271 2016-04-01T16:24:29+02:00 2025-10-14T12:54:51+02:00 2016-04-01T16:24:29+02:00 2 info:srw/schema/1/mods-v3.3xml journalArticle published yes 5 Hanna Dort author Wouter van der Bijl author Niklas Wahlberg author a69a70ff-3fff-4da8-b13a-9e8982cf63cd Sören Nylin author Christopher W. Wheat author Systematic Biology Group v1001408 department Biological Museum v1000605 department BECC: Biodiversity and Ecosystem services in a Changing Climate v1000616 department Biodiversity and Evolution v1001670 department Systematic Biology Group research group <p>Comparative analyses of gene birth–death dynamics have the potential to reveal gene families that played an important role in the evolution of morphological, behavioral, or physiological variation. Here, we used whole genomes of 30 species of butterflies and moths to identify gene birth–death dynamics among the Lepidoptera that are associated with specialist or generalist feeding strategies. Our work advances this field using a uniform set of annotated proteins for all genomes, investigating associations while correcting for phylogeny, and assessing all gene families rather than a priori subsets. We discovered that the sizes of several important gene families (e.g. those associated with pesticide resistance, xenobiotic detoxification, and/or protein digestion) are significantly correlated with diet breadth. We also found 22 gene families showing significant shifts in gene birth–death dynamics at the butterfly (Papilionoidea) crown node, the most notable of which was a family of pheromone receptors that underwent a contraction potentially linked with a shift to visual-based mate recognition. Our findings highlight the importance of uniform annotations, phylogenetic corrections, and unbiased gene family analyses in generating a list of candidate genes that warrant further exploration.</p> https://portal.research.lu.se/en/publications/2fdc22f0-0b2f-41cc-8d9b-753ac01f51e4 Oxford University Press 2024-07 eng butterflies coevolution comparative genomics diet breadth gene birth–death dynamics insect–host plant interactions Lepidoptera specialization Evolutionary Biology Genetics and Genomics 1759-6653 85198262605 38976568 10.1093/gbe/evae095 http://dx.doi.org/10.1093/gbe/evae095 16 7 evae095 https://www.scopus.com/pages/publications/85198262605 2fdc22f0-0b2f-41cc-8d9b-753ac01f51e4 2024-09-30T10:03:29+02:00 2026-05-27T22:50:01+02:00 2024-09-30T10:03:29+02:00 3 info:srw/schema/1/mods-v3.3xml book chapter published yes 1 Olivier Van Aken author b7bb7c41-9712-469e-ad54-237465e2b539 Department of Biology v1000601 department Plant Biology v1001371 department Plant Biology research group <p>This chapter discusses the current body of evidence that supports a role for mitochondria in plant cell death. In plants, a reduction of mitochondrial function and adenosine triphosphate (ATP) levels by suppression of autophagy triggered necrosis instead of developmental programmed cell death (PCD). PCD is found to be closely associated with mitochondrial reactive oxygen species (mtROS) production in plants. A key mechanism of PCD in animal systems is the excessive swelling of mitochondria; a phenomenon termed the mitochondrial permeability transition (mPT). Mitochondria are known to trigger nuclear gene expression of stress-related genes and significant evidence points towards a role for ROS in getting signals out of the mitochondria. Many pro- and antiapoptotic proteins that are associated with mitochondria were identified in non-plant systems, and a push in the plant field was initiated to find out how much of this mitochondrial pathway is conserved. Plant mitochondria become an increasingly important metabolic hub during developmental leaf senescence.</p> https://portal.research.lu.se/en/publications/58d34754-7e24-4485-b2d0-376e5b635410 Wiley 2017-01-01 eng Autophagy Developmental leaf senescence Mitochondrial permeability transition pore Mitochondrial programmed cell death pathway conservation Mitochondrial reactive oxygen species role Botany Cell Biology 9781118906576 9781118906583 85049180305 343 371 29 https://www.scopus.com/pages/publications/85049180305 58d34754-7e24-4485-b2d0-376e5b635410 2018-07-19T12:08:49+02:00 2026-05-14T12:38:20+02:00 2018-07-19T12:08:49+02:00 4 info:srw/schema/1/mods-v3.3xml journalArticle published yes 8 Guillaume Vidal author Miquel Ribas-Carbo author Marie Garmier author Guy Dubertret author Allan Rasmusson author 47c12744-58e8-4347-9bef-1b06af80e063 Chantal Mathieu author Christine H Foyer author Rosine De Paepe author Molecular Cell Biology v1000612 department Plant Biology v1001371 department Plant Biology research group Alternative oxidase (AOX) functions in stress resistance by preventing accumulation of reactive oxygen species (ROS), but little is known about in vivo partitioning of electron flow between AOX and the cytochrome pathway. We investigated the relationships between AOX expression and in vivo activity in Nicotiana sylvestris and the complex I–deficient CMSII mutant in response to a cell death elicitor. While a specific AOX1 isoform in the active reduced state was constitutively overexpressed in CMSII, partitioning through the alternative pathway was similar to the wild type. Lack of correlation between AOX content and activity indicates severe metabolic constraints in nonstressed mutant leaves. The bacterial elicitor harpin NEa induced similar timing and extent of cell death and a twofold respiratory burst in both genotypes with little change in AOX amounts. However, partitioning to AOX was increased twofold in the wild type but remained unchanged in CMSII. Oxidative phosphorylation modeling indicated a twofold ATP increase in both genotypes. By contrast, mitochondrial superoxide dismutase activity and reduced forms of ascorbate and glutathione were higher in CMSII than in the wild type. These results demonstrate genetically programmed flexibility of plant respiratory routes and antioxidants in response to elicitors and suggest that sustained ATP production, rather than AOX activity by itself or mitochondrial ROS, might be important for in planta cell death. https://portal.research.lu.se/en/publications/83f1dcf8-f240-4409-9b92-d08b9d971b94 American Society of Plant Biologists 2007 eng Biological Sciences 1040-4651 637157 000245467700023 34250672678 10.1105/tpc.106.044461 http://dx.doi.org/10.1105/tpc.106.044461 19 2 640 655 https://www.scopus.com/pages/publications/34250672678 83f1dcf8-f240-4409-9b92-d08b9d971b94 2016-04-01T12:04:51+02:00 2025-10-14T09:32:51+02:00 2016-04-01T12:04:51+02:00 5 info:srw/schema/1/mods-v3.3xml journalArticle published yes 4 Martina Holst author 285f31fc-2454-4393-9c42-a110791479b2 Veronica Johansson author eef559da-7069-4560-a6f2-f32d254e08a9 Kersti Alm author 7da78877-3e96-4e0c-8999-d24ca7a3c947 Stina Oredsson author a8f39329-4536-42b1-a5b9-e93a9df7f3eb Functional zoology v1000610 department Department of Biology v1000601 department The spermine analogue N(1),N(11)-diethylnorspermine (DENSPM) efficiently depletes the polyamine pools in the breast cancer cell line L56Br-C1 and induces apoptotic cell death via the mitochondrial pathway. In this study, we have over-expressed the anti-apoptotic protein Bcl-2 in L56Br-C1 cells and investigated the effect of DENSPM treatment. DENSPM-induced cell death was significantly reduced in Bcl-2 over-expressing cells. Bcl-2 over-expression reduced DENSPM-induced release of the pro-apoptotic proteins AIF, cytochrome c, and Smac/DIABLO from the mitochondria. Bcl-2 over-expression reduced the DENSPM-induced activation of caspase-3. Bcl-2 over-expression also prevented DENSPM-induced Bax cleavage and reduction of Bcl-X(L) and survivin levels. The DENSPM-induced activation of the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase was reduced by Bcl-2 over-expression, partly preventing polyamine depletion. Thus, Bcl-2 over-expression prevented a number of DENSPM-induced apoptotic effects https://portal.research.lu.se/en/publications/9d500204-c53d-41df-9152-232b555aebea Elsevier 2008 eng Apoptosis Spermine analogue Cytochrome c Human breast cancer Bcl-2 Zoology 1095-8355 744472 000260586200009 39049171988 17920946 10.1016/j.cellbi.2007.08.011 http://dx.doi.org/10.1016/j.cellbi.2007.08.011 yes 32 66 74 https://www.scopus.com/pages/publications/39049171988 9d500204-c53d-41df-9152-232b555aebea 2016-04-01T11:44:31+02:00 2025-10-14T11:49:55+02:00 2016-04-01T11:44:31+02:00 6 info:srw/schema/1/mods-v3.3xml journalArticle published yes 3 Cecilia Hegardt author fd7ecf49-39fd-463a-8f45-854d0d55404e Gunnar Andersson author Stina Oredsson author a8f39329-4536-42b1-a5b9-e93a9df7f3eb Breastcancer-genetics v1000472 department Functional zoology v1000610 department Two experimental systems representative of the mitochondrial and death receptor apoptotic pathways are the dexamethasone-induced programmed cell death in mouse thymocytes and the antibody-mediated cross-ligation of the Fas receptor in the human leukemic T-cell line Jurkat, respectively. In both cell systems, caspase-9, -8, and -3 were activated upon induction of apoptosis and a sub-G(1) peak appeared as a sign of ongoing DNA fragmentation. Addition of 1 mM spermine together with dexamethasone inhibited caspase activation and the appearance of the sub-G(1) peak in mouse thymocytes. In contrast, Fas-induced cell death was totally unaffected by spermine addition. Spermine addition significantly elevated the spermine concentration in both thymocytes and Jurkat cells. Thus, spermine per se did not inhibit the caspases but rather their activation. The fact that spermine inhibited caspase activation only in the thymocytes implies that spermine inhibited dexamethasone-induced apoptosis upstream of caspase-9 activation. https://portal.research.lu.se/en/publications/7e34990a-62ec-42cd-a9a1-d1119cd1e118 Academic Press 2001 eng glucocorticoid apoptosis Fas death receptor thymocytes Jurkat cells sub-G1 peak cell cycle phase distribution polyamines caspases flow cytometry Cancer and Oncology 1090-2422 1120285 11399061 0034949763 10.1006/excr.2001.5230 http://dx.doi.org/10.1006/excr.2001.5230 yes 266 2 333 341 https://www.scopus.com/pages/publications/0034949763 7e34990a-62ec-42cd-a9a1-d1119cd1e118 2016-04-01T12:37:17+02:00 2025-10-14T13:11:00+02:00 2016-04-01T12:37:17+02:00 7 info:srw/schema/1/mods-v3.3xml journalArticle published yes 4 Veronica Johansson author eef559da-7069-4560-a6f2-f32d254e08a9 Iréne Thuvesson author b1b8f3b7-c89b-444a-a594-d375e794dd29 Kersti Alm author 7da78877-3e96-4e0c-8999-d24ca7a3c947 Stina Oredsson author a8f39329-4536-42b1-a5b9-e93a9df7f3eb Department of Biology v1000601 department Division of Hematology and Clinical Immunology v1000553 department Molecular Cell Biology v1000612 department Functional zoology v1000610 department The retinoblastoma protein (pRb) pathway is frequently altered in breast cancer cells. pRb is involved in the regulation of cell proliferation and cell death. The breast cancer cell line L56Br-C1 does not express pRb and is extremely sensitive to treatment with the polyamine analogue N (1),N (11)-diethylnorspermine (DENSPM) which causes apoptosis. Polyamines are essential for the regulation of cell proliferation, cell differentiation and cell death. DENSPM depletes cells of polyamines, e.g., by inducing the activity of the polyamine catabolic enzyme spermidine/spermine N (1)-acetyltransferase (SSAT). In this study, L56Br-C1 cells were transfected with human pRb-cDNA. Overexpression of pRb inhibited DENSPM-induced cell death and DENSPM-induced SSAT activity. This suggests that the pRb protein level is a promising marker for polyamine depletion sensitivity and that there is a connection between pRb and the regulation of SSAT activity. We also show that SSAT protein levels and SSAT activity do not always correlate, suggesting that there is an unknown regulation of SSAT https://portal.research.lu.se/en/publications/38d0b841-32e1-44b2-93c7-406fde202871 Springer 2012 eng Hematology http://www.ncbi.nlm.nih.gov/pubmed/21809081?dopt=Abstract yes 0939-4451 2151616 000299506000049 21809081 84861657647 10.1007/s00726-011-1007-y http://dx.doi.org/10.1007/s00726-011-1007-y yes 42 929 937 https://www.scopus.com/pages/publications/84861657647 The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Division of Hematology and Transfusion Medicine (013041100), Animal Physiology (Closed 2011) (011011000), Functional Zoology (432112239), Molecular Cell Biology (432112241) 38d0b841-32e1-44b2-93c7-406fde202871 2016-04-04T07:04:03+02:00 2025-10-14T12:23:59+02:00 2016-04-04T07:04:03+02:00 8 info:srw/schema/1/mods-v3.3xml journalArticle published yes 6 Esther Nobs author c0f32e7d-a434-4316-9f2f-3cd77fb11b4b Katie Laschanzky author eda2b4d4-2cd7-40ca-bee5-49eae19de0a1 Kristina Munke author 0e58fbfb-566a-46e4-b435-63625cd3a6c2 Elin Movert author 197e0d86-c703-4f7c-9468-3a0ad33de54e Christine Valfridsson author 0f7b1df4-8534-4986-bb37-3503d7f2fdac Fredric Carlsson author e231010b-9421-4978-8123-2421d1931ebb Evolutionary Ecology and Infection Biology v1001669 department Functional zoology v1000610 department Microbiology Group v1001372 department Mucosal Immunology v1000403 department Department of Biology v1000601 department Infectious Immunology v1000371 department Microbiology Group research group Mucosal Immunology research group Infectious Immunology research group <p>UNLABELLED: Serine protease inhibitors (serpins) constitute the largest family of protease inhibitors expressed in humans, but their role in infection remains largely unexplored. In infected macrophages, the mycobacterial ESX-1 type VII secretion system permeabilizes internal host membranes and causes leakage into the cytosol of host DNA, which induces type I interferon (IFN) production via the cyclic GMP-AMP synthase (cGAS) and stimulator of IFN genes (STING) surveillance pathway, and promotes infection in vivo. Using the Mycobacterium marinum infection model, we show that ESX-1-mediated type I IFN signaling in macrophages selectively induces the expression of serpina3f and serpina3g, two cytosolic serpins of the clade A3. The membranolytic activity of ESX-1 also caused leakage of cathepsin B into the cytosol where it promoted cell death, suggesting that the induction of type I IFN comes at the cost of lysosomal rupture and toxicity. However, the production of cytosolic serpins suppressed the protease activity of cathepsin B in this compartment and thus limited cell death, a function that was associated with increased bacterial growth in infected mice. These results suggest that cytosolic serpins act in a type I IFN-dependent cytoprotective feedback loop to counteract the inevitable toxic effect of ESX-1-mediated host membrane rupture.</p><p>IMPORTANCE: The ESX-1 type VII secretion system is a key virulence determinant of pathogenic mycobacteria. The ability to permeabilize host cell membranes is critical for several ESX-1-dependent virulence traits, including phagosomal escape and induction of the type I interferon (IFN) response. We find that it comes at the cost of lysosomal leakage and subsequent host cell death. However, our results suggest that ESX-1-mediated type I IFN signaling selectively upregulates serpina3f and serpina3g and that these cytosolic serpins limit cell death caused by cathepsin B that has leaked into the cytosol, a function that is associated with increased bacterial growth in vivo. The ability to rupture host membranes is widespread among bacterial pathogens, and it will be of interest to evaluate the role of cytosolic serpins and this type I IFN-dependent cytoprotective feedback loop in the context of human infection.</p> https://portal.research.lu.se/en/publications/60d7913b-f9db-477b-bb83-a3796a23058b American Society for Microbiology 2024-09-11 eng Animals Female Mice Bacterial Proteins/metabolism Cell Death Cytosol/microbiology Feedback, Physiological Host-Pathogen Interactions Interferon Type I/metabolism Macrophages/microbiology Mice, Inbred C57BL Mycobacterium Infections, Nontuberculous/microbiology Mycobacterium marinum/pathogenicity Serpins/metabolism Signal Transduction Type VII Secretion Systems/metabolism Microbiology in the Medical Area 2161-2129 39087767 85203872794 10.1128/mbio.00384-24 http://dx.doi.org/10.1128/mbio.00384-24 15 9 e0038424 https://www.scopus.com/pages/publications/85203872794 60d7913b-f9db-477b-bb83-a3796a23058b 2024-10-10T15:52:54+02:00 2026-05-24T13:47:37+02:00 2024-10-10T15:52:54+02:00 9 info:srw/schema/1/mods-v3.3xml journalArticle published yes 4 H. R. Momeni author M. Soleimani Mehranjani author M. H. Abnosi author Martin Kanje author bee3a1d8-0a92-47f8-b36f-d3fabbb0557b Functional zoology v1000610 department Organotypic spinal cord slices from neonatal mammals could be a powerful model for evaluation of cell survival but also cell death mechanisms. The aim of this study was to establish an in vitro model for investigating cell survival and mechanism involved in cell death in neonatal spinal cord slices. The spinal cord was sliced and incubated into culture medium. The MTT assay was carried out to assess the viability of the slices and fluorescent staining was used to study morphological features of apoptosis, where as nucleosomal DNA fragmentation was detected using agarose gel electrophoresis. The results of the present study demonstrated that the slices could be maintained in culture up to 14 days. Both neurons and glial cells died by apoptosis and application of a general caspase inhibitor neither affected slice survival nor nucleosomal DNA fragmentation after 24 h in culture. In addition, the inhibitor failed to block apoptosis in neurons and glial cells in the cultured slices. Our results suggest that in the cultured slices, apoptosis is the main reason for neuron and glial cell death, which occurs by a caspase-independent mechanism. https://portal.research.lu.se/en/publications/55a63191-5cfc-4248-a5fb-59572f5d8c4c Springer Science and Business Media B.V. 2008 eng neonatal mouse Apoptosis MTT assay spinal cord slices Zoology 1028-6276 1476281 000269358700003 70350325645 32 A2 109 116 https://www.scopus.com/pages/publications/70350325645 55a63191-5cfc-4248-a5fb-59572f5d8c4c 2016-04-01T13:27:51+02:00 2026-01-03T17:08:46+01:00 2016-04-01T13:27:51+02:00 10 info:srw/schema/1/mods-v3.3xml journalArticle published yes 2 Olivier Van Aken author b7bb7c41-9712-469e-ad54-237465e2b539 Barry James Pogson author Department of Biology v1000601 department Plant Biology v1001371 department Plant Biology research group <p>The energy-converting organelles mitochondria and chloroplasts are tightly embedded in cellular metabolism and stress response. To appropriately control organelle function, extensive regulatory mechanisms are at play that involve two-way exchange between the nucleus and mitochondria/chloroplasts. In recent years, our understanding of how mitochondria and chloroplasts provide â € retrograde' feedback to the nucleus, resulting in targeted transcriptional changes, has greatly increased. Nevertheless, mitochondrial and chloroplast retrograde signalling have largely been studied independently, and only few points of interaction have been found or proposed. Through reassessment of recent publications, this perspective proposes that two of the most well-studied retrograde signalling pathways in plants, those mediated by ANAC017 and those mediated by phosphoadenosine phosphate (PAP), are most likely convergent and can direct overlapping genes. Furthermore, at least part of this common retrograde response appears targeted towards suppression of programmed cell death (PCD) triggered by organellar defects. The identified target genes are discussed in light of their roles in PCD suppression and amplifying the signalling cascade via positive-feedback loops. Finally, a mechanism is proposed that may explain why the convergence of PAP/ANAC017-dependent signalling appears capable of suppressing some types of PCD lesions, but not others, based on the subcellular location of the initial PCD-inducing dysfunction.</p> https://portal.research.lu.se/en/publications/64d5b01e-b765-4dd9-b184-80a8b6a5f385 Springer Nature 2017-06-01 eng Cell Biology 1350-9047 85019940742 28498364 000401701800003 10.1038/cdd.2017.68 http://dx.doi.org/10.1038/cdd.2017.68 yes 24 6 955 960 6 https://www.scopus.com/pages/publications/85019940742 64d5b01e-b765-4dd9-b184-80a8b6a5f385 2017-06-14T12:40:13+02:00 2026-04-30T20:15:31+02:00 2017-06-14T12:40:13+02:00 11 info:srw/schema/1/mods-v3.3xml journalArticle published yes 1 Per Ekström author fbf66dc2-8f5a-4e22-847c-b2ef0f83d09f Functional zoology v1000610 department <p>Analogous to the death of developing neurones deprived of trophic factors, nerve injury in adult life could lead to nerve cell death by apoptosis. Here the occurrence of apoptotic mouse sciatic sensory neurones after injury was investigated by nick-labelling DNA breaks. A small proportion of the neurones reliably became apoptotic after injury in vivo. The response was strongly amplified when the nerves were injured in vitro, where Ca²⁺-chelation and protein synthesis inhibition were effective in inhibiting apoptosis. In addition to nerve cells, both Schwann cells and satellite cells became apoptotic after injury. Apoptosis in cultured mouse sciatic nerves appears advantageous for the identification of survival factors acting on adult peripheral neurones.</p> https://portal.research.lu.se/en/publications/0886ae3e-c728-4f94-9edd-71ede32da36f Lippincott Williams & Wilkins 1995 eng Apoptosis Mammalian Nerve regeneration Peripheral nerve Programmed cell death Schwann cell proliferation Cell Biology Neurosciences 0959-4965 0029039160 7632888 6 7 1029 1032 https://www.scopus.com/pages/publications/0029039160 yes 0886ae3e-c728-4f94-9edd-71ede32da36f 2016-12-07T14:49:24+01:00 2026-01-12T23:42:08+01:00 2016-12-07T14:49:24+01:00 12 info:srw/schema/1/mods-v3.3xml journalArticle published yes 3 Martyna Broda author A. Harvey Millar author Olivier Van Aken author b7bb7c41-9712-469e-ad54-237465e2b539 Molecular Cell Biology v1000612 department Plant Biology v1001371 department Plant Biology research group <p>Mitophagy is a conserved cellular process that is important for autophagic removal of damaged mitochondria to maintain a healthy mitochondrial population. Mitophagy also appears to occur in plants and has roles in development, stress response, senescence, and programmed cell death. However, many of the genes that control mitophagy in yeast and animal cells are absent from plants, and no plant proteins marking defunct mitochondria for autophagic degradation are yet known. New insights implicate general autophagy-related proteins in mitophagy, affecting the senescence of plant tissues. Mitophagy control and its importance for energy metabolism, survival, signaling, and cell death in plants are discussed. Furthermore, we suggest mitochondrial membrane proteins containing ATG8-interacting motifs, which might serve as mitophagy receptor proteins in plant mitochondria.</p> https://portal.research.lu.se/en/publications/df6dcd25-1b3d-4de0-8d4b-bee2de13a1f8 Elsevier 2018-05 eng autophagy cell death mitochondria plant hormones reactive oxygen species senescence Botany Cell Biology 1360-1385 85044310533 29576328 10.1016/j.tplants.2018.02.010 http://dx.doi.org/10.1016/j.tplants.2018.02.010 yes 23 5 434 450 https://www.scopus.com/pages/publications/85044310533 df6dcd25-1b3d-4de0-8d4b-bee2de13a1f8 2018-04-10T06:51:11+02:00 2026-03-19T01:41:14+01:00 2018-04-10T06:51:11+02:00 13 info:srw/schema/1/mods-v3.3xml journalArticle published yes 5 Koichi Takao author Mattias Rickhag author 4edd8db7-ccff-4abe-9c16-9326d1cf7d38 Cecilia Hegardt author fd7ecf49-39fd-463a-8f45-854d0d55404e Stina Oredsson author a8f39329-4536-42b1-a5b9-e93a9df7f3eb Lo Persson author 820d297d-9777-4c7c-aee6-897792170c33 Section IV v1000445 department Breastcancer-genetics v1000472 department Functional zoology v1000610 department Biogenic Amines v1000357 department Biogenic Amines research group https://portal.research.lu.se/en/publications/c4358dcf-6e68-4b19-af6e-f239f2fc4067 https://portal.research.lu.se/files/4731822/625269.pdf application/pdf 156434 no Elsevier 2006 eng Other Clinical Medicine Basic Medicine http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16406751&dopt=Abstract yes 1878-5875 150401 000235705100014 16406751 30944447512 16406751 10.1016/j.biocel.2005.10.020 http://dx.doi.org/10.1016/j.biocel.2005.10.020 yes 38 4 621 628 https://www.scopus.com/pages/publications/30944447512 The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Department of Experimental Medical Science (013210000), Functional Zoology (432112239), Department of Clinical Sciences, Lund (013230000), Biogenic Amines (013212037), Oncology, MV (013035000), Laboratory for Experimental Brain Research (013041000) c4358dcf-6e68-4b19-af6e-f239f2fc4067 2016-04-01T16:38:16+02:00 2025-10-26T15:47:14+01:00 2016-04-01T16:38:16+02:00 14 info:srw/schema/1/mods-v3.3xml theses published Department of Cell and Organism Biology, Animal Physiology. Building Lecture hall, Helgonavägen 3B, Lund, Sweden 1 HamidReza Momeni author 917c9ab8-2b01-4f46-af1c-bca64691d5f0 Martin Kanje supervisor bee3a1d8-0a92-47f8-b36f-d3fabbb0557b Prof. Sven Tågerud opponent Department of Chemistry and Biomedical Sciences, University of Kalmar, Kalmar, Sweden. Department of Biology v1000601 department Motor neuron degeneration is a critical phenomenon during spinal cord injuries and some neurodegenerative diseases. However, the mechanisms by which cell death is induced in these neurons are poorly understood. One reason for this, is the lack of model systems in which the survival and death of adult motor neurons can be studied under controlled conditions. This thesis is an attempt to develop such a model system. Here, we tried to establish an in vitro model utilizing slices of adult mouse spinal cord.<br/><br> <br/><br> A respiratory assay (MTT) was used to assess cell viability in the slices, and cell death was evaluated by morphological features using fluorescent nuclear stains or biochemical feature of cell death using agarose gel electrophoresis of DNA.<br/><br> <br/><br> We could demonstrate that both slice thickness and the presence of serum in the culture medium affected slice survival. By using the optimal conditions, we showed that survival could be maintained in the slice cultures for a few days. In the cultured slices, both motor neurons and glial cells died by apoptosis. Interestingly, apoptosis was induced independent of caspase activation, excitotoxicity or free radical formation-classical inducers of apoptosis. Immunohistochemical studies revealed that two isoforms of the Ca2+ -dependent proteases, calpain I and calpain II, appeared in the nuclei of the motor neurons in response to injury and culturing. Calpain activation occurred both in the cytoplasm and the nuclei of the motor neurons as assessed by a fluorogenic calpain substrate. Calpain activation was also observed in the slices by Western blotting using an antibody to 150-kD calpain-cleaved ?-fodrin fragment. Calpain inhibitors and chelation of Ca2+ by EGTA delayed apoptosis and prevented calpain activation in the motor neurons. In contrast, the general caspase inhibitor Z-VAD.fmk had no effect on either apoptosis or calpain activation in the motor neurons.<br/><br> <br/><br> In conclusion, our results show that massive caspase-independent but calpain-dependent apoptosis is induced in motor neurons in response to injury and culturing and that inhibitors of calpain can delay apoptosis in the motor neurons of cultured slices. https://portal.research.lu.se/en/publications/856569d2-dc03-48e4-8090-a7482961439b Department of Cell and Organism Biology, Lund University 2006 eng Calpain Djurfysiologi Animal physiology Spinal cord Organ culture Mouse Motor neurons Caspase Calpain inhibitor Calpain activity Apoptosis Biological Sciences 91-85067-25-3 546762 110 2006-06-02T09:00:00+02:00 <div class="article_info">Hamid R. Momeni and Martin Kranje. <span class="article_issue_date"></span>. <span class="article_title">Apoptosis is induced in cultured adult spinal cord slices from mouse by caspase- and glutamate independent mechanisms.</span> (submitted)</div> <div class="article_info">Hamid R. Momeni and Martin Kranje. <span class="article_issue_date">2005</span>. <span class="article_title">The calpain inhibitor VI prevents apoptosis of adult motor neurons.</span> <span class="journal_series_title">Neuroreport</span>, <span class="journal_pages">pp 1065-1068</span>.</div> <div class="article_info">Hamid R. Momeni, Seifollah Azadi and Martin Kranje. <span class="article_issue_date"></span>. <span class="article_title">Calpain activation and apoptosis in motor neurons of cultured adult mouse spinal cord slices.</span> (submitted)</div> <div class="article_info">Hamid R. Momeni and Martin Kranje. <span class="article_issue_date">2006</span>. <span class="article_title">Calpain inhibitors delay injury-induced apoptosis in adult mouse spinal cord motor neurons.</span> <span class="journal_series_title">Neuroreport</span>, (inpress)</div> The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Department of Cell and Organism Biology (Closed 2011.) (011002100), Animal Physiology (Closed 2011) (011011000) 856569d2-dc03-48e4-8090-a7482961439b 2016-04-04T11:06:53+02:00 2025-04-04T15:30:37+02:00 2016-04-04T11:06:53+02:00 15 info:srw/schema/1/mods-v3.3xml journalArticle published yes 5 Sonia Kleindorfer author Katharina J. Peters author Georgina Custance author Rachael Dudaniec author 9631ae65-60dc-4e0e-810a-e2460051228a Jody A. O'Connor author MEMEG v1000611 department Molecular Ecology and Evolution Lab v1001405 department Molecular Ecology and Evolution Lab research group The conservation behavior framework is useful to identify key linkages between behavior and conservation practice. We apply this framework to a novel host-parasite system on the Galapagos Islands and ask if there have been changes in parasite oviposition behavior and host mortality patterns across the first decade (2004-2013) of its known association. The Dipteran parasite Philornis downsi was first discovered in Darwin's finch nests in 1997 and is the biggest threat to the survival of Galapagos land birds. Host mortality has increased over the past decade. In Dipterans, pupation and pupae size are determined by access to host resources. Here, we test the hypothesis that P. downsi flies are laying eggs in finch nests earlier in the nestling phase to maximize larval feeding time and therefore chance of pupation success before host death. The results show fewer 1st instar larvae later in the host nesting cycle in support of earlier egg laying behavior by female flies. Between 2004 and 2013, parasite intensity increased from similar to 28 to similar to 48 parasites per nest, host mortality increased from similar to 50% to similar to 90%, and host age at death decreased from similar to 11 to similar to 5 days. The earlier age at host death was correlated with fewer pupae (from similar to 50% to similar to 20%) and smaller pupae size (similar to 10% decrease). Changes in parasite behavior reveal new fitness costs to both the parasite and Darwin's finches. These findings underscore the need for urgent conservation action to save Darwin's finches from extinction due to a novel, lethal and introduced parasite https://portal.research.lu.se/en/publications/4d443617-9072-4469-bd3a-fec4b2417968 Oxford University Press 2014 eng Host mortality Parasite size Darwin's finches Ectoparasitism Camarhynchus Geospiza Biological Sciences 1674-5507 4652887 000340840700012 84905680483 60 4 542 550 https://www.scopus.com/pages/publications/84905680483 4d443617-9072-4469-bd3a-fec4b2417968 2016-04-01T13:35:15+02:00 2025-10-14T11:01:39+02:00 2016-04-01T13:35:15+02:00 16 info:srw/schema/1/mods-v3.3xml journalArticle published yes 5 Martina Holst author 285f31fc-2454-4393-9c42-a110791479b2 Johan Staaf author 5f4154d5-0276-4115-82cd-fa0181f1d209 Göran B Jönsson author ac0b4551-a9d6-47f0-ba3d-3075acac22e4 Cecilia Hegardt author fd7ecf49-39fd-463a-8f45-854d0d55404e Stina Oredsson author a8f39329-4536-42b1-a5b9-e93a9df7f3eb Functional zoology v1000610 department Breastcancer-genetics v1000472 department Polyamine analogue treatment results in growth inhibition and sometimes in cell death. Therefore, polyamine analogues are considered in the treatment of cancer; however, the cellular properties that govern sensitivity are not known. The objective of this study was to elucidate molecular mechanisms behind apoptosis induced by the polyamine analogue N, N-diethylnorspermine (DENSPM). Four different breast cancer cell lines were treated with DENSPM. Cell death was evaluated with flow cytometry and a caspase 3 assay. The levels of a number of proapoptotic and antiapoptotic proteins in subcellular compartments were evaluated with western blot. In the most sensitive cell line, DENSPM treatment induced the release of cytochrome c from mitochondria, resulting in activation of caspase 3 but without decreasing the mitochondrial transmembrane potential. However, in the three other cell lines DENSPM treatment did not induce extensive cell death. This is partly explained by the high levels of antiapoptotic proteins Bcl-2 and Bad and low levels of proapoptotic proteins Bax and procaspase 3 in these three cell lines. The results are also partly explained by the degree of activation of the catabolic enzyme spermidine/spermine-N-acetyltransferase and polyamine pool reduction achieved by DENSPM treatment. Our results show that the protein profile of proapoptotic and antiapoptotic proteins may contribute to the outcome to treatment with the polyamine analogue DENSPM. The results also indicate that it should be possible to find molecular markers for sensitivity to DENSPM that could be used in the clinic to predict sensitivity to a polyamine analogue. https://portal.research.lu.se/en/publications/337d13eb-6afc-463a-9d7e-0a7a7ec7f1e0 Lippincott Williams & Wilkins 2008 eng Cancer and Oncology http://www.ncbi.nlm.nih.gov/pubmed/18766001?dopt=Abstract yes 0959-4973 1243465 000259521900004 52649141739 18766001 10.1097/CAD.0b013e32830f902b http://dx.doi.org/10.1097/CAD.0b013e32830f902b yes 19 9 871 883 https://www.scopus.com/pages/publications/52649141739 337d13eb-6afc-463a-9d7e-0a7a7ec7f1e0 2016-04-04T07:35:19+02:00 2025-10-14T13:14:41+02:00 2016-04-04T07:35:19+02:00 17 info:srw/schema/1/mods-v3.3xml journalArticle published yes 10 François Maillard author 21641b2d-0b97-44dd-b80b-b414d2a3a6df Danny Lopes Ramos author b46c254d-5a6e-47b5-a899-0aab847b2136 Bowen Zhang author c90655a0-50a9-41eb-b7eb-168b7af6b29f Ashish Ahlawat author 50f9a624-f701-4516-bc4c-e4b1db7b4e9b Allison L. Gill author Carl Troein author 8189bbae-c13a-432d-a7b2-b08a40b5a22d Mattias Hedenström author Tobias Sparrman author Per Persson author ca05969a-f748-4577-a918-51f43655bce1 Anders Tunlid author 69b1412f-ca6f-4391-ae5d-0c9ff7332866 Microbial Ecology v1001404 department Microbial Biogeochemistry in Lund v1001485 department BECC: Biodiversity and Ecosystem services in a Changing Climate v1000616 department Department of Earth and Environmental Sciences (MGeo) v1001772 department Centre for Environmental and Climate Science (CEC) v1000615 department Computational Science for Health and Environment v1001703 department Microbial Ecology research group Microbial Biogeochemistry in Lund research group Computational Science for Health and Environment research group <p>Fungal necromass is increasingly recognized as a major component of soil organic matter, and identifying the factors that govern its formation is critical for understanding and predicting the global carbon cycle. Among these factors, the biochemical composition of mycelial residues at senescence, particularly melanin content, has been consistently identified as a key determinant of the fraction of fungal necromass that persists in soils. However, even non-melanized mycelial residues exhibit a recalcitrant fraction that resists microbial decomposition, and the reasons for this persistence are not well understood. To address this gap, we asked whether the growth stage at which a single non-melanized fungal species dies governs the decay of its necromass in soil. Using Neurospora crassa , we produced seven necromass types that ranged from early exponential growth to prolonged starvation and decomposed them in forest soil. Necromass derived from biomass experiencing net growth at the time of harvest decomposed up to ten times faster than necromass from starved cultures, which were undergoing biomass loss. By the end of decomposition, only about 10 % of necromass from early-growth-stage biomass remained, while nearly 65 % of necromass from starved biomass persisted. Differences in mycelial biochemical traits, particularly C:N ratio and the degree of branching of glucans, which varied with fungal growth stage at death, explained variation in both decay rates and the size of the persistent fractions. Our findings suggest that the growth stage of fungi at death is a key factor driving fungal necromass decay profiles, with potentially large consequences for the contribution of fungal necromass to soil organic matter stocks.</p> https://portal.research.lu.se/en/publications/abcea3e5-ecf2-48fc-bee7-4564dc943c3c Elsevier 2026-03 eng FTIR Fungal cell wall Fungal necromass NMR Organic matter decomposition Raman spectroscopy Soil Science Forest Science Environmental Sciences and Nature Conservation (including Biodiversity) 0038-0717 105026125306 10.1016/j.soilbio.2025.110079 http://dx.doi.org/10.1016/j.soilbio.2025.110079 214 110079 Publisher Copyright: © 2025 The Authors. abcea3e5-ecf2-48fc-bee7-4564dc943c3c 2026-03-09T10:20:06+01:00 2026-03-10T03:51:00+01:00 2026-03-09T10:20:06+01:00 18 info:srw/schema/1/mods-v3.3xml journalArticle published general 2 Ingvar Kärnefelt author ee1fcd6a-1ce4-410d-8fec-920dc123714e Patrik Frödén author ee77513b-4524-441d-929d-425acf69a771 Botanical collections v1000606 department Biodiversity v1000603 department Erik Acharius, Linnaeus last pupil and accounted as "The father of lichenology", was born 250 years ago, on the 10th of October 1757. After graduating in Uppsala and taking his medical degree in Lund, he eventually settled in Vadstena, where he worked as a provincial doctor and chief physician at the hospital for veneral diseases. At the age of 36 he wrote his first lichenological work and then continued to work relentlessly on lichen systematics until his death in 1819, expanding the knowledge of this group enormously. He described many new species and genera which still are recognized, and his lichen system was recognized worldwidely. After his death a series of unfortunate events led to that his valuable lichen herbarium was sold to Helsinki. The majority of the herbarium, though, was donated to Lund university in 1843, and we are proud to preserve this in the Biological museums today. https://portal.research.lu.se/en/publications/2da29634-40fa-4110-8a37-fdb275f47a09 Svenska Linnésällskapet, Uppsala, Svenska Linnésällskapet, Uppsala 2007 eng Ecology (including Biodiversity Conservation) Botany 0375-2038 744421 105 131 2da29634-40fa-4110-8a37-fdb275f47a09 2016-04-01T16:09:00+02:00 2025-04-04T14:30:18+02:00 2016-04-01T16:09:00+02:00 19 info:srw/schema/1/mods-v3.3xml conference abstract published yes 6 Neivis Tormo-Badia author 16bbcc4c-1d4e-4221-a1af-5f3e5765a51c Caroline Bolmeson author ec7e1391-d285-40dd-820d-f12c9b23d1b7 Maria Carlsén author 96515ea4-b669-485e-b0a9-6857950df814 Anna Makowska author 2c4e9379-5fcd-4057-8fcc-da1ba02147e8 Shafqat Ahmad author ff0d772f-2808-4216-a97c-16b61da9ecdf Corrado Cilio author 1ebd674c-8298-40c8-8558-1178e1362eae Diabetes - Immunovirology v1000488 department Create Health v1000177 department Evolutionary ecology v1000609 department Department of Clinical Sciences, Malmö v1000476 department EXODIAB: Excellence of Diabetes Research in Sweden v1001241 department 46th Annual Meeting of the European-Association-for-the- Study-of-Diabetes (EASD) Diabetes - Immunovirology research group https://portal.research.lu.se/en/publications/ee274cc0-57d5-4834-9d12-96cd53b0884b Springer 2010 2010-09-20 - 2010-09-24 eng Endocrinology and Diabetes 1432-0428 1727735 000280689700420 10.1007/s00125-010-1872-z http://dx.doi.org/10.1007/s00125-010-1872-z yes 53 Suppl. 1 419 419 The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Cellular Autoimmunity Unit (013241520), Evolutionary Ecology (432112238), Endocrinology (013241500), Create Health (000080030), Pediatrics/Urology/Gynecology/Endocrinology (013240400) ee274cc0-57d5-4834-9d12-96cd53b0884b 2016-04-01T11:10:53+02:00 2025-04-04T14:26:40+02:00 2016-04-01T11:10:53+02:00 20 1.1(department exact v1000601 or popularscience exact 0) and deathandordepartmentexactv1000601popularscienceexactsrw.ServerChoicescrdeath