The NK gene complex is a region on human chromosome 12 containing several families of lectin‐like genes including the CD94 and NKG2 NK receptor genes. We report here that the region telomeric of CD94 contains in addition to the LOX‐1 gene the novel human DECTIN‐1 and the CLEC‐1 and CLEC‐2 genes within about 100 kb. Sequence similarities and chromosomal arrangement suggest that these genes form a separate subfamily of lectin‐like genes within the NK gene complex. DECTIN‐1 is selectively expressed in dendritic cells and to a lowerextent in monocytes and macrophages. mRNA forms with and without a stalk exon are observed. During functional maturation of dendritic cells the level of DECTIN‐1 mRNA is down‐regulated several‐fold. CLEC‐1 is found to be not only expressed in dendritic cells, but also in endothelial cells and in the latter aspect resembles the LOX‐1 gene. Whereas recombinant full‐length DECTIN‐1 and LOX‐1 are transported to the cell surface, CLEC‐1 proteins accumulate in perinuclear compartments. We propose that this family of lectin‐like genes encodes receptors with important immune and/or scavenger functions in monocytic, dendritic and endothelial cells.

The expression of the ANR1 MADS-box gene was manipulated in transgenic plants to investigate its role in the NO(3)(-)-dependent regulation of root development in Arabidopsis thaliana. Constitutive overexpression of ANR1 in roots, achieved using GAL4 enhancer trap lines, resulted in more rapid early seedling development, increased lengths and numbers of lateral roots and increased shoot fresh weight. Based on results obtained with five different enhancer trap lines, the overexpression of ANR1 in the lateral root tips appears to be more important for this phenotype than its level of expression in the developing lateral root primordia. Dexamethasone-mediated induction of ANR1 in lines expressing an ANR1-GR (glucocorticoid receptor) fusion protein stimulated lateral root growth but not primary root growth. Short-term (24 h) dexamethasone treatments led to prolonged stimulation of lateral root growth, whether the lateral roots were already mature or still unemerged at the time of treatment. In split-root experiments, localized application of dexamethasone to half of the root system of an ANR1-GR line elicited a localized increase in both the length and numbers of lateral roots, mimicking the effect of a localized NO(3)(-) treatment. In both types of transgenic line, the root phenotype was strongly dependent on the presence of NO(3)(-), indicating that there are additional components involved in ANR1 function that are NO(3)(-) regulated. The implications of these results for our understanding of ANR1's mode of action in the root response to localized NO(3)(-) are discussed.

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The production by filamentous fungi of therapeutic glycoproteins intended for use in mammals is held back by the inherent difference in protein N-glycosylation and by the inability of the fungal cell to modify proteins with mammalian glycosylation structures. Here, we report protein N-glycan engineering in two Aspergillus species. We functionally expressed in the fungal hosts heterologous chimeric fusion proteins containing different localization peptides and catalytic domains. This strategy allowed the isolation of a strain with a functional ␣-1,2-mannosidase producing increased amounts of N-glycans of the Man 5 GlcNAc 2 type. This strain was further engineered by the introduction of a functional GlcNAc transferase I construct yielding GlcNAcMan 5 GlcNac 2 N-glycans. Additionally, we deleted algC genes coding for an enzyme involved in an early step of the fungal glycosylation pathway yielding Man 3 GlcNAc 2 N-glycans. This modification of fungal glycosylation is a step toward the ability to produce humanized complex N-glycans on therapeutic proteins in filamentous fungi.