Woody plants are characterised by a highly complex vascular system, wherein the secondary xylem (wood) is responsible for the axial transport of water and various substances. Previous studies have focused on the dead conductive elements in this heterogeneous tissue. However, the living xylem parenchyma cells, which constitute a significant functional fraction of the wood tissue, have been strongly neglected in studies on tree biology. Although there has recently been increased research interest in xylem parenchyma cells, the mechanisms that operate in these cells are poorly understood. Therefore, the present review focuses on selected roles of xylem parenchyma and its relevance in wood functioning. In addition, to elucidate the importance of xylem parenchyma, we have compiled evidence supporting the hypothesis on the significance of parenchyma cells in tree functioning and identified the key unaddressed questions in the field.

The shoot apical meristem (SAM) ensures continuous plant growth and organogenesis. In LD 30 °C, plants lacking AtFTSH4, an ATP-dependent mitochondrial protease that counteracts accumulation of internal oxidative stress, exhibit a puzzling phenotype of premature SAM termination. We aimed to elucidate the underlying cellular and molecular processes that link AtFTSH4 with SAM arrest. We studied AtFTSH4 expression, internal oxidative stress accumulation, and SAM morphology. Directly in the SAM we analysed H₂O₂ accumulation, mitochondria behaviour, and identity of stem cells using WUS/CLV3 expression. AtFTSH4 was expressed in proliferating tissues, particularly during the reproductive phase. In the mutant, SAM, in which internal oxidative stress accumulates predominantly at 30 °C, lost its meristematic fate. This process was progressive and stage-specific. Premature meristem termination was associated with an expansion in SAM area, where mitochondria lost their functionality. All these effects destabilised the identity of the stem cells. SAM termination in ftsh4 mutants is caused both by internal oxidative stress accumulation with time/age and by the tissue-specific role of AtFTSH4 around the flowering transition. Maintaining mitochondria functionality within the SAM, dependent on AtFTSH4, is vital to preserving stem cell activity throughout development.

Shoot and root apical meristems (SAM and RAM, respectively) are crucial to provide cells for growth and organogenesis and therefore need to be maintained throughout the life of a plant. However, plants lacking the mitochondrial protease AtFTSH4 exhibit an intriguing phenotype of precocious cessation of growth at both the shoot and root apices when grown at elevated temperatures. This is due to the accumulation of internal oxidative stress and progressive mitochondria dysfunction. To explore the impacts of the internal oxidative stress on SAM and RAM functioning, we study the expression of selected meristem-specific (STM, CLV3, WOX5) and cell cycle-related (e.g., CYCB1, CYCD3;1) genes at the level of the promoter activity and/or transcript abundance in wild-type and loss-of-function ftsh4-1 mutant plants grown at 30 °C. In addition, we monitor cell cycle progression directly in apical meristems and analyze the responsiveness of SAM and RAM to plant hormones. We show that growth arrest in the ftsh4-1 mutant is caused by cell cycle dysregulation in addition to the loss of stem cell identity. Both the SAM and RAM gradually lose their proliferative activity, but with different timing relative to CYCB1 transcriptional activity (a marker of G2-M transition), which cannot be compensated by exogenous hormones.

In the shoot apical meristem (SAM) of Arabidopsis, PIN1-dependent polar auxin transport (PAT) regulates two crucial developmental processes: organogenesis and vascular system formation. However, the knockout mutation in the PIN1 gene does not fully inhibit these two processes. Therefore, we investigated a potential source of auxin for organogenesis and vascularization during inflorescence stem development. We analyzed auxin distribution in wild-type (WT) and pin1 mutant plants using a refined protocol of auxin immunolocalization; auxin activity, with the response reporter pDR5:GFP; and expression of auxin biosynthesis genes YUC1 and YUC4. Our results revealed that regardless of the functionality of PIN1-mediated PAT, auxin is present in the SAM and vascular strands. In WT plants, auxin always accumulates in all cells of the SAM, whereas in pin1 mutants, its localization within the SAM changes ontogenetically and is related to changes in the structure of the vascular system, organogenic activity of SAM, and expression levels of YUC1 and YUC4 genes. Our findings indicate that the presence of auxin in the meristem of pin1 mutants is an outcome of at least two PIN1-independent mechanisms: acropetal auxin transport from differentiated tissues with the use of vascular strands and auxin biosynthesis within the SAM.