{"messages":[{"status":"ok","category":"all"}], "collection":[{"title":"Marchantia stem cell maintenance and re-establishment are controlled by MpPIN1-mediated auxin transport and ARF signalling","authors":"Bonter, I.;Rebmann, M.;Delmans, M.;Romani, F.;Haseloff, J.","author_corresponding":"Jim Haseloff","author_corresponding_institution":"University of Cambridge, Department of Plant Sciences","doi":"10.64898\/2026.06.29.735252","date":"2026-6-30","version":"1","type":"new results","license":"cc_by_nc","category":"Plant Biology","jatsxml":"https:\/\/www.biorxiv.org\/content\/early\/2026\/6-\/0\/2026.06.29.735252.source.xml","abstract":"\n                \n                  Meristem organization in land plants depends on coordinated auxin distribution, transport and response, yet how these processes are integrated during vegetative growth of the gametophyte of non-seed plants remains poorly understood. Here, we describe dissection of the auxin network in the liverwort\n                  Marchantia polymorpha\n                  using a suite of endogenous and synthetic reporters. Quantitative imaging with the R2DII auxin response sensor revealed that the apical meristem is positioned at a stable auxin minimum, with auxin levels increasing toward differentiated tissues. This spatial configuration correlates with polar localization of the auxin efflux carrier MpPIN1 along the direction of auxin flux. Disruption of Mp\n                  PIN1\n                  alters auxin distribution and compromises tissue regeneration, but does not prevent initial meristem formation, indicating that PIN-mediated transport reinforces rather than defines stem-cell niche identity. Imaging of auxin response reporters and Mp\n                  ARF1\n                  and Mp\n                  ARF2\n                  knock-in reporters further revealed a constrained auxin response within the meristem, characterized by low auxin signalling, dependent on the inhibitory activity of Mp\n                  ARF2\n                  in the stem cell zone. During regeneration, transient, oscillatory\n                  ARF\n                  dynamics were observed before stabilization of a new auxin minimum and re-establishment of normal meristem architecture. Together, our results are consistent with auxin responses in the Marchantia meristem being shaped by an incoherent feed-forward network topology that couples auxin flux, transcriptional constraint and niche permissiveness. This architecture provides a robust framework for stem-cell maintenance and re-establishment, revealing ancestral principles of meristem regulation in land plants.\n                \n                \n                  SUMMARY STATEMENT\n                  \n                    By mapping hormone distribution at cellular resolution in the liverwort\n                    Marchantia polymorpha\n                    , we reveal fundamental principles governing how plants maintain and rebuild their stem cell niches.\n                  \n                ","funder":"NA","published":"NA","server":"bioRxiv"},{"title":"Seasonal climatic impacts on orchid productivity in an urban ecosystem","authors":"Brundrett, M.","author_corresponding":"Mark C Brundrett","author_corresponding_institution":"University of Western Australia","doi":"10.64898\/2026.06.29.735162","date":"2026-6-30","version":"1","type":"new results","license":"cc_by_nd","category":"Plant Biology","jatsxml":"https:\/\/www.biorxiv.org\/content\/early\/2026\/6-\/0\/2026.06.29.735162.source.xml","abstract":"\n                \n                  Context\n                  The global diversity hotspot in Southwest Australia has >480 orchids facing increasing threats from climate extremes, fire and habitat decline.\n                \n                \n                  Aims\n                  To develop effective and consistent tools for measuring climate impacts on productivity in a diverse urban orchid community.\n                \n                \n                  Methods\n                  Annual variations in flower and seed production for 17 orchids were determined using thousands of records over a decade with extreme climate variability.\n                \n                \n                  Key results\n                  Rainfall deficits and temperatures in autumn, winter and spring increased substantially over 125 years. Seasonal climate anomalies reduced flowering and seed production for orchids, but this varied between species and seasons. These effects were summarised by climate response (CRI) and sensitivity (CSI) indexes. Early or late flowering species were most vulnerable to seasonal drought, and visually deceptive pollination preferred warm dry conditions. CRIs were strongly correlated with orchid pollination syndromes and flowering times. Effects on mycorrhizal fungi and pollinators were also observed. Extrapolating climate trends to 2100 predicted further impacts on orchid productivity (-5-40%).\n                \n                \n                  Conclusions\n                  Orchid climate responses were diverse and deeply integrated with pollination, phenology, fire sensitivity and other key traits.\n                \n                \n                  Implications\n                  Research in an urban climate observatory produced a climate analysis framework that is likely relevant to many orchids and other biota.\n                ","funder":"NA","published":"NA","server":"bioRxiv"},{"title":"AlphaFold-Multimer reveals diverse cyclin-CDK substrate docking interactions","authors":"Willich, S.;Kapadia, N.;Nurse, P.","author_corresponding":"Sarah Willich","author_corresponding_institution":"The Francis Crick Institute","doi":"10.64898\/2026.06.29.735189","date":"2026-6-30","version":"1","type":"new results","license":"cc_by_nc_nd","category":"Cell Biology","jatsxml":"https:\/\/www.biorxiv.org\/content\/early\/2026\/6-\/0\/2026.06.29.735189.source.xml","abstract":"\n                \n                  Cyclin-dependent kinases (CDKs) control eukaryotic cell-cycle progression by phosphorylating specific substrates with substrate recognition often involving cyclin-specific docking interactions. However, in minimal cell cycle control systems driven by a single cyclin-CDK complex, how docking interactions contribute to the differential timing of substrate phosphorylation remains unclear. Here, we used AlphaFold-Multimer to systematically predict interactions between the fission yeast mitotic cyclin-CDK fusion Cdc13-L-Cdc2 and its known\n                  in vivo\n                  CDK substrates. We found that many substrates are predicted to interact with the cyclin hydrophobic patch, and have identified a previously uncharacterised docking motif, [FVIPWGLAM](x)xER[LMV] (ERL motif), with features consistent with an atypical RxL motif. We show that ERL motifs can functionally substitute for canonical RxL motifs to promote phosphorylation of a model CDK substrate by Cdc13-Cdc2, while the S-phase cyclin-CDK Cig2-Cdc2 was found to preferentially phosphorylate substrates containing canonical RxL motifs. Finally, we investigated whether Cdc13-L-Cdc2 is predicted to preferentially bind DNA replication substrates over mitotic substrates but found no evidence of differential binding. These results reveal diversity in cyclin-CDK substrate recognition beyond established docking motifs.\n                ","funder":"NA","published":"NA","server":"bioRxiv"},{"title":"Species-dependent accumulation of PsaA in etioplasts points to light-independent steps in Photosystem I biogenesis","authors":"W\u0119grzyn, A.;Wardak, K.;Mazur, R.;Go\u0142\u0119biewska, K.;Gawro\u0144ski, P.;Kowalewska, ?.","author_corresponding":"\u0141ucja Kowalewska","author_corresponding_institution":"Uniwersytet Warszawski","doi":"10.64898\/2026.06.25.734457","date":"2026-6-30","version":"1","type":"new results","license":"cc_by","category":"","jatsxml":"https:\/\/www.biorxiv.org\/content\/early\/2026\/6-\/0\/2026.06.25.734457.source.xml","abstract":"\n                Whether Photosystem I (PSI) core subunits accumulate prior to light exposure in developing angiosperm seedlings remains unresolved, with conflicting reports across species. Here, we investigated the presence and membrane colocalization of the PSI core subunit PsaA in etioplasts of dark-grown angiosperms representing dicot and monocot species. Immunoblotting showed that PsaA accumulates in etioplasts of all three dicot species examined (pea, Arabidopsis, and runner bean), whereas in the monocot oat it was detected only after prolonged etiolation, at substantially lower levels and with an anomalously high apparent molecular weight. Blue-native PAGE analysis reveals that a fraction of PsaA co-migrates with LPOR, PsaB, FNR, and chlorophyll synthase, suggesting co-localization within a shared membrane microdomain rather than stable complex formation. The thylakoid insertase Alb3 was more abundant in dicot etioplasts, consistent with a potential role in the early integration of PsaA into the membrane. Upon illumination, pea reached PSI functionality faster than oat, with P700 oxidation detectable 30 min earlier, linking the dark accumulation of PsaA to an accelerated photosynthetic onset. These findings demonstrate light-independent accumulation of a PSI core subunit in a species-dependent manner and point to early steps in PSI biogenesis that precede full photosynthetic complex assembly.\n                \n                  Highlight\n                  Contrary to prevailing models, a Photosystem I core subunit PsaA accumulates in dark-grown angiosperm seedlings before light exposure, revealing light-independent early steps in photosynthetic complex biogenesis.\n                ","funder":"NA","published":"NA","server":"bioRxiv"},{"title":"LDB1-dependent enhancer connectivity defines T-cell leukemia identities and masks metabolic vulnerabilities","authors":"Bhansali, R.;Long, J.;Polonen, P.;Isobe, T.;Wang, S.;Zhang, S.;Geng, Z.;Tausif, A.;Antopia, M.;Aboreden, N.;Skuli, S.;Giardine, B.;Keller, C.;Hardison, R.;Tan, K.;Mullighan, C.;Blobel, G.","author_corresponding":"Rahul S Bhansali","author_corresponding_institution":"Division of Hematology and Oncology, Department of Medicine, Hospital of the University of Pennsylvania; Division of Hematology, The Childrens Hospital of Phila","doi":"10.64898\/2026.06.29.733236","date":"2026-6-30","version":"1","type":"new results","license":"cc_no","category":"Cancer Biology","jatsxml":"https:\/\/www.biorxiv.org\/content\/early\/2026\/6-\/0\/2026.06.29.733236.source.xml","abstract":"\n                Spatial enhancer connectivity is fundamental to proper gene regulation. Enhancer dysregulation has emerged as a hallmark of cancers, including T-cell acute lymphoblastic leukemias (T-ALL). T-ALL are aggressive malignancies characterized by marked transcriptional heterogeneity driven by distinct stages of developmental arrest and diverse noncoding alterations. How these cancers co-opt nuclear architecture to rewire enhancer connectivity remains poorly understood. Here, we report that the LDB1 chromatin architectural complex is an essential mediator of enhancer-oncogene looping that sustains oncogenic transcriptional programs across multiple T-ALL subtypes. Integrating bulk and single-cell transcriptomic data from patients with T-ALL and healthy hematopoietic controls, we show that the LDB1-dependent regulatory circuitry defines the molecular identities of distinct T-ALL subtypes while restricting plasticity toward alternative cell states. LDB1 loss dismantles chromatin looping among cell state-defining enhancers liberating them to form promiscuous interactions with nearby genes. This enhancer rewiring stimulates expression of key metabolic genes, creating a mevalonate pathway dependency exploitable with statin treatment. Our study establishes LDB1 as a central executor of T-ALL regulatory circuitry and more broadly illustrates chromatin rewiring as a source of targetable dependencies in cancer.","funder":"NA","published":"NA","server":"bioRxiv"}]}