Search

The pericarp is the predominant tissue determining the structural characteristics of most fruits. However, the molecular and genetic mechanisms controlling pericarp development remain only partially understood. Previous studies have identified that CLASS-II KNOX genes regulate fruit size, shape, and maturation in Arabidopsis thaliana and Solanum lycopersicum. Here we characterized the roles of the S. lycopersicum CLASS-II KNOX (TKN-II) genes in pericarp development via a detailed histological, anatomical, and karyotypical analysis of TKN-II gene clade mRNA-knockdown (35S:amiR-TKN-II) fruits. We identify that 35S:amiR-TKN-II pericarps contain more cells around their equatorial perimeter and fewer cell layers than the control. In addition, the cell sizes but not the ploidy levels of these pericarps were dramatically reduced. Further, we demonstrate that fruit shape and pericarp layer number phenotypes of the 35S:amiR-TKN-II fruits can be overridden by the procera mutant, known to induce a constitutive response to the plant hormone gibberellin. However, neither the procera mutation nor exogenous gibberellin application can fully rescue the reduced pericarp width and cell size phenotype of 35S:amiR-TKN-II pericarps. Our findings establish that TKN-II genes regulate tomato fruit anatomy, acting via gibberellin to control fruit shape but utilizing a gibberellin-independent pathway to control the size of pericarp cells.

The pericarp is the predominant tissue determining the structural characteristics of most fruits. However, the molecular and genetic mechanisms controlling pericarp development remain only partially understood. Previous studies have identified that CLASS-II KNOX genes regulate fruit size, shape, and maturation inArabidopsis thalianaandSolanum lycopersicum. Here we characterized the roles of theSolanum lycopersicumCLASS-II KNOX (TKN-II) genes in pericarp development via a detailed histological, anatomical, and karyotype analysis of theTKN-IIknockdown (35S:amiR-TKN-II) fruits. We identify that35S:amiR-TKN-IIpericarps contain more cells around their equatorial perimeter and fewer cell layers than the control. In addition, the cell sizes but not the ploidy levels of these pericarps were dramatically reduced.Further, we demonstrate that fruit shape and pericarp layer number phenotypes of the35S:amiR-TKN-IIfruits can be overridden by theproceramutant, known to induce a constitutive response to the plant hormone gibberellin. However, neither theproceramutation nor exogenous gibberellin application can fully rescue the reduced pericarp width and cell size phenotype of35S:amiR-TKN-IIpericarps. Our findings establish that TKN-II genes regulate tomato fruit anatomy, acting via gibberellin to control fruit shape but utilizing a gibberellin-independent pathway to control the size of pericarp cells.HighlightTomatoCLASS-II KNOXgenes regulate fruit and pericarp anatomy via GA-dependent and independent pathways.

Plants continuously form new organs in different developmental contexts in response to environmental cues. Underground lateral roots initiate from prepatterned cells in the main root, but cells can also bypass the root-shoot trajectory separation and generate shoot-borne roots through an unknown mechanism. We mapped tomato ( Solanum lycopersicum ) shoot-borne root development at single-cell resolution and showed that these roots initiate from phloem-associated cells through a unique transition state. This state requires the activity of a transcription factor that we named SHOOTBORNE ROOTLESS ( SBRL ) . Evolutionary analysis reveals that SBRL ’s function and cis regulation are conserved in angiosperms and that it arose as an ancient duplication, with paralogs controlling wound-induced and lateral root initiation. We propose that the activation of a common transition state by context-specific regulators underlies the plasticity of plant root systems.

During plant post-embryonic growth new meristems and associated stem cells form in different development contexts in order to respond to environmental cues. While underground lateral roots initiate from designated cells in the main root, an unknown mechanism allows cells to bypass the root/shoot identity trajectory and generate shoot-borne-roots. Using single-cell profiling of tomato (Solanum lycoperiscum) stems we isolated a rare transient cell population that serve as progenitors for shoot-borne-root meristems. Analysis of this population identified a transcription factor required for the formation of shoot-borne-roots which we named SHOOT BORNE ROOTLESS (SBRL). Evolutionary analysis revealed that SBRL function is deeply conserved in angiosperms and that it arose as part of an ancient duplicated superlocus, only lost in root-less plants, containing both shoot-borne and lateral root initiation regulators. We propose that the ability to activate a common transition state with context-specific regulators allows the remarkable developmental plasticity found in plants.One Sentence SummaryHighly conserved superlocus of LBD genes, acting within an early transition identity, regulates shoot-borne and lateral root formation.

The root meristem can regenerate following removal of its stem-cell niche by recruitment of remnant cells from the stump. Regeneration is initiated by rapid accumulation of auxin near the injury site but the source of this auxin is unknown. Here, we show that auxin accumulation arises from the activity of multiple auxin biosynthetic sources that are newly specified near the cut site and that their continuous activity is required for the regeneration process. Auxin synthesis is highly localized while PIN-mediated transport is dispensable for auxin accumulation and tip regeneration. Roots lacking the activity of the regeneration competence factor ERF115, or that are dissected at a zone of low regeneration potential, fail to activate local auxin sources. Remarkably, restoring auxin supply is sufficient to confer regeneration capacity to these recalcitrant tissues. We suggest that regeneration competence relies on the ability to specify new local auxin sources in a precise temporal pattern.

Following removal of its stem cell niche, the root meristem can regenerate by recruitment of remnant cells from the stump. Regeneration is initiated by rapid accumulation of auxin near the injury site but the source of this auxin is unknown. Here, we show that auxin accumulation arises from the activity of multiple auxin biosynthetic sources that are newly specified near the cut site and that their continuous activity is required for the regeneration process. Auxin synthesis is highly localized and PIN-mediate transport is dispensable for auxin accumulation and tip regeneration. Roots lacking the activity of the regeneration competence factorERF115, or that are dissected at a zone of low-regeneration potential, fail to activate local auxin sources. Remarkably, restoring auxin supply is sufficient to confer regeneration capacity to these recalcitrant tissues. We suggest that regeneration competence relies on the ability to specify new local auxin sources in a precise spatio-temporal pattern.

Hematopoietic stem and progenitor cells (HSPCs) are a small population of undifferentiated cells that have the capacity for self-renewal and differentiate into all blood cell lineages. These cells are the most useful cells for clinical transplantations and for regenerative medicine. So far, it has not been possible to expand adult hematopoietic stem cells (HSCs) without losing their self-renewal properties. CD74 is a cell surface receptor for the cytokine macrophage migration inhibitory factor (MIF), and its mRNA is known to be expressed in HSCs. Here, we demonstrate that mice lacking CD74 exhibit an accumulation of HSCs in the bone marrow (BM) due to their increased potential to repopulate and compete for BM niches. Our results suggest that CD74 regulates the maintenance of the HSCs and CD18 expression. Its absence leads to induced survival of these cells and accumulation of quiescent and proliferating cells. Furthermore, in in vitro experiments, blocking of CD74 elevated the numbers of HSPCs. Thus, we suggest that blocking CD74 could lead to improved clinical insight into BM transplant protocols, enabling improved engraftment., Hematopoietic stem and progenitor cells (HSPCs) can self-renew and differentiate into all blood cell lineages, making them useful for clinical transplantations and regenerative medicine. This study shows that blocking the MIF receptor CD74 increases the accumulation of HSPCs and could improve the efficacy of bone marrow transplantation protocols.

CD74 is a type II cell surface protein that was previously shown to play a role in antigen presentation and as a receptor for the cytokine macrophage migration inhibitory factor (MIF). Studies from recent years demonstrate an important role for CD74 in maintenance of innate and adaptive immune cells. This chapter discusses the MIF/CD74-dependent role in regulating cell survival, metabolism, adhesion, and response to hypoxia in health and disease.

CD74 is a cell-surface receptor for the cytokine macrophage migration inhibitory factor. Macrophage migration inhibitory factor binding to CD74 induces its intramembrane cleavage and the release of its cytosolic intracellular domain (CD74-ICD), which regulates cell survival. In the present study, we characterized the transcriptional activity of CD74-ICD in chronic lymphocytic B cells. We show that following CD74 activation, CD74-ICD interacts with the transcription factors RUNX (Runt related transcription factor) and NF-κB and binds to proximal and distal regulatory sites enriched for genes involved in apoptosis, immune response, and cell migration. This process leads to regulation of expression of these genes. Our results suggest that identifying targets of CD74 will help in understanding of essential pathways regulating B-cell survival in health and disease.