Despite the growing body of work on molecular components required for regenerative repair,we still lack a deep understanding of the ability of some animal species to regenerate their appropriate complex anatomical str...Despite the growing body of work on molecular components required for regenerative repair,we still lack a deep understanding of the ability of some animal species to regenerate their appropriate complex anatomical structure following damage.A key question is how regenerating systems know when to stop growth and remodeling-what mechanisms implement recognition of correct morphology that signals a stop condition?In this work,we review two conceptual models of pattern regeneration that implement a kind of pattern memory.In the first one,all cells communicate with each other and keep the value of the total signal received from the other cells.If a part of the pattern is amputated,the signal distribution changes.The difference fromthe original signal distribution stimulates cell proliferation and leads to pattern regeneration,in effect implementing an error minimization process that uses signaling memory to achieve pattern correction.In the second model,we consider a more complex pattern organization with different cell types.Each tissue contains a central(coordinator)cell that controls the tissue and communicates with the other central cells.Each of them keeps memory about the signals received from other central cells.The values of these signals depend on the mutual cell location,and the memory allows regeneration of the structure when it is modified.The purpose of these models is to suggest possible mechanisms of pattern regeneration operating on the basis of cell memory which are compatible with diverse molecular implementation mechanisms within specific organisms.展开更多
Major life transitions are always difficult because change costs energy.Recent findings have demonstrated how mitochondrial oxidative phosphorylation(OxPhos)defects increase the energetic cost of living and that exces...Major life transitions are always difficult because change costs energy.Recent findings have demonstrated how mitochondrial oxidative phosphorylation(OxPhos)defects increase the energetic cost of living and that excessive integrated stress response(ISR)signaling may prevent cellular identity transitions during development.In this perspective,we discuss general bioenergetic principles of life transitions and the costly molecular processes involved in reprograming the cellular hardware/software as cells shift identity.The energetic cost of cellular differentiation has not been directly quantified,representing a gap in knowledge.We propose that the ISR is an energetic checkpoint evolved to(i)prevent OxPhos-deficient cells from engaging in excessively costly transitions and(ii)allow ISR-positive cells to recruit systemic energetic resources by signaling via GDF15 and the brain.展开更多
Disagreements about language use are common both between and within fields.Where interests require multidisciplinary collaboration or the field of research has the potential to impact society at large,it becomes criti...Disagreements about language use are common both between and within fields.Where interests require multidisciplinary collaboration or the field of research has the potential to impact society at large,it becomes critical to minimize these disagreements where possible.The development of diverse intelligent systems,regardless of the substrate(e.g.,silicon vs.biology),is a case where both conditions are met.Significant advancements have occurred in the development of technology progressing toward these diverse intelligence systems.Whether progress is silicon based,such as the use of large language models,or through synthetic biology methods,such as the development of organoids,a clear need for a community-based approach to seeking consensus on nomenclature is now vital.Here,we welcome collaboration from the wider scientific community,proposing a pathway forward to achieving this intention,highlighting key terms and fields of relevance,and suggesting potential consensus-making methods to be applied.展开更多
基金support of the G.Harold and Leila Y.Mathers Charitable Foundationthe Templeton World Charity Foundation(TWCF0089/AB55)the W.M.Keck Foundation
文摘Despite the growing body of work on molecular components required for regenerative repair,we still lack a deep understanding of the ability of some animal species to regenerate their appropriate complex anatomical structure following damage.A key question is how regenerating systems know when to stop growth and remodeling-what mechanisms implement recognition of correct morphology that signals a stop condition?In this work,we review two conceptual models of pattern regeneration that implement a kind of pattern memory.In the first one,all cells communicate with each other and keep the value of the total signal received from the other cells.If a part of the pattern is amputated,the signal distribution changes.The difference fromthe original signal distribution stimulates cell proliferation and leads to pattern regeneration,in effect implementing an error minimization process that uses signaling memory to achieve pattern correction.In the second model,we consider a more complex pattern organization with different cell types.Each tissue contains a central(coordinator)cell that controls the tissue and communicates with the other central cells.Each of them keeps memory about the signals received from other central cells.The values of these signals depend on the mutual cell location,and the memory allows regeneration of the structure when it is modified.The purpose of these models is to suggest possible mechanisms of pattern regeneration operating on the basis of cell memory which are compatible with diverse molecular implementation mechanisms within specific organisms.
基金supported by grants from the NIH(R01MH119336,R01MH122706,R01AG066828,and RF1AG076821)the Wharton Fund,and the Baszucki Brain Research Fund to M.P.M.L.gratefully acknowledges support from the Templeton World Charity Foundation(TWCF0606)the Bill and Melinda Gates Foundation.
文摘Major life transitions are always difficult because change costs energy.Recent findings have demonstrated how mitochondrial oxidative phosphorylation(OxPhos)defects increase the energetic cost of living and that excessive integrated stress response(ISR)signaling may prevent cellular identity transitions during development.In this perspective,we discuss general bioenergetic principles of life transitions and the costly molecular processes involved in reprograming the cellular hardware/software as cells shift identity.The energetic cost of cellular differentiation has not been directly quantified,representing a gap in knowledge.We propose that the ISR is an energetic checkpoint evolved to(i)prevent OxPhos-deficient cells from engaging in excessively costly transitions and(ii)allow ISR-positive cells to recruit systemic energetic resources by signaling via GDF15 and the brain.
基金A.B.received funding from Economic and Social Research Council grant ES/T01279X/1 to support involvement in this work.
文摘Disagreements about language use are common both between and within fields.Where interests require multidisciplinary collaboration or the field of research has the potential to impact society at large,it becomes critical to minimize these disagreements where possible.The development of diverse intelligent systems,regardless of the substrate(e.g.,silicon vs.biology),is a case where both conditions are met.Significant advancements have occurred in the development of technology progressing toward these diverse intelligence systems.Whether progress is silicon based,such as the use of large language models,or through synthetic biology methods,such as the development of organoids,a clear need for a community-based approach to seeking consensus on nomenclature is now vital.Here,we welcome collaboration from the wider scientific community,proposing a pathway forward to achieving this intention,highlighting key terms and fields of relevance,and suggesting potential consensus-making methods to be applied.