Developmental and environmental effects on the expression of the C3-C4 intermediate phenotype in moricandia arvensis

Cellular anatomy and expression of glycine decarboxylase (GDC) protein were studied during leaf development of the C3-C4 intermediate species Moricandia arvensis. Leaf anatomy was initially C3-like and the number and profile area of mitochondria in the bundle-sheath cells were the same as those in adjacent mesophyll cells. Between a leaf length of 6 and 12 mm there was a bundle-sheath-specific, 4-fold increase in the number of mitochondrial profiles, followed by a doubling of their individual profile areas as the leaves expanded further. Subunits of GDC were present in whole-leaf extracts before the anatomical development of bundle-sheath cells. Whereas the GDC H-protein content of leaves increased steadily throughout development, the increase in GDC P-protein was synchronous with the development of mitochondria in the bundle sheath. The P-protein was confined to bundle-sheath mitochondria throughout leaf development, and its content in individual mitochondria increased before the anatomical development of the bundle sheath. Anatomical and biochemical attributes of the C3-C4 character were present in the cotyledons and sepals but not in other photosynthetic organs/tissues. In leaves and cotyledons that developed in the dark, the expression of the P-protein and the organellar development were reduced but the bundle-sheath cell specificity was retained.

The eli1 mutation reveals a link between cell expansion and secondary cell wall formation in Arabidopsis thaliana.

Mutants with altered patterns of lignification have been identified in a population of mutagenised Arabidopsis seedlings. One of the mutants exhibited ectopic lignification (eli) of cells throughout the plant that never normally lignify. The reduced expansion of eli1 cells resulted in a stunted phenotype, and xylem cells were misshapen and failed to differentiate into continuous strands, causing a disorganized xylem. Analysis of phenotypes associated with double mutants of eli1 lit (lion's tail), a cell expansion mutant, indicated that the primary defect in eli1 plants may be inappropriate initiation of secondary wall formation and subsequent aberrant lignification of cells caused by altered cell expansion. Related ectopic lignification phenotypes were also observed in other cell expansion mutants, suggesting a mechanism that senses cell size and controls subsequent secondary wall formation. Interactions between eli1 and wol (woodenleg), a mutant altering xylem cell specification, revealed a role for ELI1 in promoting formation of continuous xylem strands, and demonstrated that ELI1 functions during cell elongation zone in the primary root and other tissues.