Amazing grass: developmental genetics of maize domestication.

Crop plants were domesticated by prehistoric farmers through artificial selection to provide a means of feeding the human population. This article discusses the developmental genetics of crop domestication and improvement, including the historical framework and recent approaches in maize and other grasses. In many cases, selecting for a plant form that correlates with productivity involves controlling meristem activity. In the domestication of modern maize from its progenitor Zea mays ssp. parviglumis, QTL (quantitative trait loci) mapping, genetics and population genomics approaches have identified several genes that contain signatures of selection. Only a few genes involved in the derivation of the highly productive maize ear have been identified, including teosinte glume architecture1 and ramosa1. Future prospects hinge on forward and reverse genetics, as well as on other approaches from the developing discipline of evo-devo (evolutionary developmental biology).

Shoot meristem size is dependent on inbred background and presence of the maize homeobox gene, knotted1.

The knotted1 (kn1) gene of maize is expressed in meristems and is absent from leaves, including the site of leaf initiation within the meristem. Recessive mutations of kn1 have been described that limit the capacity to make branches and result in extra carpels. Dominant mutations suggest that kn1 function plays a role in maintaining cells in an undifferentiated state. We took advantage of a Ds-induced dominant allele in order to screen for additional recessive alleles resulting from mobilization of the Ds element. Analysis of one such allele revealed a novel embryonic shoot phenotype in which the shoot initiated zero to few organs after the cotyledon was made, resulting in plants that arrested as seedlings. We refer to this phenotype as a limited shoot. The limited shoot phenotype reflected loss of kn1 function, but its penetrance was background dependent. We examined meristem size and found that plants lacking kn1 function had shorter meristems than non-mutant siblings. Furthermore, meristems of restrictive inbreds were significantly shorter than meristems of permissive inbreds, implying a correlation between meristem height and kn1 gene function in the embryo. Analysis of limited shoot plants during embryogenesis indicated a role for kn1 in shoot meristem maintenance. We discuss a model for kn1 in maintenance of the morphogenetic zone of the shoot apical meristem.

Production and structure elucidation of di- and oligosaccharide lipids (biosurfactants) from Tsukamurella sp. nov.

The bacterium Tsukamurella sp. nov., isolated from soil, was found to produce novel glycolipids when grown on sunflower oil as the sole carbon source. The glycolipids were isolated by chromatography on silica columns and their structures elucidated using a combination of multidimensional NMR and MS techniques. The three main components are 2,3-di-O-acyl-alpha-D-glucopyranosyl-(1-1)-alpha-D-glucopyranose, 2,3-di-O-acyl-beta-D-glucopyranosyl-(1-2)-4,6-di-O-acyl-alpha-D- glucopyranosyl-(1-1)-alpha-D-glucopyranose and 2,3-di-O-acyl-beta-D-glucopyranosyl-(1-2)-beta-D-galactopyranosyl- (1-6)-4,6-di-O-acyl-alpha-D-glucopyranosyl-(1-1)-alpha-D- glucopyranosyl which are linked to fatty acids varying in chain length from C4 to C18. The glycolipids are mainly extracellular but are also found attached to the cell walls. During the cultivation the composition of the glycolipids changed from disaccharide- to tri- and tetrasaccharide lipids. The glycolipids show good surface-active behaviour and have antimicrobial properties.

Sequence analysis and expression patterns divide the maize knotted1-like homeobox genes into two classes.

The homeobox of the knotted1 (kn1) gene was used to isolate 12 related sequences in maize. The homeodomains encoded by the kn1-like genes are very similar, ranging from 55 to 89% amino acid identity. Differences outside the precisely conserved third helix allowed us to group the genes into two classes. The homeodomains of the seven class 1 genes share 73 to 89% identical residues with kn1. The four class 2 genes share 55 to 58% identical residues with kn1, although the conservation within the class is greater than 87%. Expression patterns were analyzed by RNA gel blot analysis. Class 1 genes were highly expressed in meristem-enriched tissues, such as the vegetative meristem and ear primordia. Expression was not detectable in leaves. The class 2 genes were expressed in all tissues, although one was abundantly expressed in roots. The genes were mapped using recombinant inbred populations. We determined that clusters of two to three linked genes are present on chromosomes 1 and 8; otherwise, the genes are distributed throughout the genome. Four pairs of genes, similar in both sequence and expression patterns, mapped within duplicated regions of the genome.

The developmental gene Knotted-1 is a member of a maize homeobox gene family.

The Knotted-1 (Kn1) locus is defined by several dominant gain-of-function mutations that alter leaf development. Foci of cells along the lateral veins do not differentiate properly, but continue to divide, forming outpocketings or knots. The ligule, a fringe normally found at the junction of leaf blade and sheath, is often displaced and perpendicular to its normal position. The phenotype is manifested in all cell layers of the leaf blade, but is controlled by a subgroup of cells of the inner layer. Mutations result from the insertion of transposable elements or a tandem duplication. We show that the Kn1 gene encodes a homeodomain-containing protein, the first identified in the plant kingdom. Sequence comparisons strongly suggest that Kn1 acts as a transcription factor. Here we use the Kn1 homeobox to isolate other expressed homeobox genes in maize. The Kn1 homeobox may permit the isolation of genes that, like animal and fungal counterparts, regulate cell fate determination.

A tandem duplication causes the Kn1-O allele of Knotted, a dominant morphological mutant of maize.

Molecular and genetic techniques are used to define Kn1-O, a mutation which interferes with the normal differentiation of vascular tissue in leaves. Sequences associated with a previously cloned allele, Kn1-2F11, were used as hybridization probes in a Southern analysis of Kn1-O. By this analysis, Kn1-O lacks the Ds2 transposable element that causes Kn1-2F11 but instead is associated with a sequence duplication. Sequence and restriction analysis of genomic clones show that the duplication consists of a tandem array of two 17-kb repeats. Analysis of Kn1-O derivatives indicates that the duplication itself conditions the mutant phenotype; a severely knotted line, Kn1-Ox, has gained a repeat unit to form a triplication, whereas normal derivatives have either lost a repeat unit or sustained insertions that disrupt the tandem duplication. These insertions map near the central junction of the tandem duplication, suggesting that the mutant phenotype results from the novel juxtaposition of sequences. We discuss models that relate the tandem duplication of sequences to altered gene expression.

Cloning Knotted, the dominant morphological mutant in maize using Ds2 as a transposon tag.

The Kn1-2F11 mutation causes protrusions or knots along the lateral veins of the first few leaves of the maize plant. The phenotype is visible when an unlinked gene, presumably Ac, is present in the genome. The mutation is closely linked to a genetically unstable Adh1 mutation that resulted from the insertion of a Ds2 element (Döring et al., 1984; Chen et al., 1986). Using a unique sequence from the Ds2 element as a hybridization probe, a genomic restriction fragment that cosegregated with the knotted phenotype was cloned. It carries the Kn1-2F11 locus by the following criteria. (i) Cosegregation of the fragment is tightly linked to the phenotype. (ii) Somatic and germinal excision produce a fragment which is the expected size of a revertant fragment; progeny containing the revertant size fragment are normal. (iii) The sequences that hybridize to this fragment are significantly altered in the chromosome containing the original knotted mutation, Kn1-O, (iv) The cloned fragment does not hybridize to a chromosome that contains a deletion of Kn1-O.