Biomedical subjects

Z P Wills

Publications and source records attributed to Z P Wills.

3 recordsLinked to original sources

PubMed1998

Drosophila Rac1 controls motor axon guidance.

Previous genetic studies of intersegmental nerve b development have identified several cell-surface proteins required for correct axon guidance to appropriate target muscles. Here we provide evidence that the small GTPase Drac1 also plays a key role in this guidance process. Neuronal expression of the dominant negative mutation Drac1(N17) causes axons to bypass and extend beyond normal synaptic partners. This phenotype is consistently reproduced by pharmacological blockade of actin assembly. Genetic interactions between Drac1(N17) and the receptor-tyrosine phosphatase Dlar suggest that intersegmental nerve b guidance requires the integration of multiple, convergent signals.

Actins↗

PubMed1995

Coding sequence composition flanking either signal element alters V(D)J recombination efficiency.

Lymphoid V(D)J rearrangement is targeted by recombination signal sequences (RSS) bordering V, D or J exons. We demonstrate that the DNA composition of flanking coding positions, particularly poly(A) or poly(T) stretches at one or both RSS, diminishes V(D)J recombination up to 100-fold. Positionally correct cleavages occur in the inhibited reactions, since the junctions formed show the same frequency of precision as uninhibited reactions. Open/shut cleavage/rejoining is not increased at a normal RSS in substrates containing inhibitory A/T homopolymers versus random sequence at a second RSS. Thus recombinase action at both cleavage sites is severely disrupted by modified coding sequences.

B-Lymphocytes↗

PubMed1993

V(D)J recombination coding junction formation without DNA homology: processing of coding termini.

Coding junction formation in V(D)J recombination generates diversity in the antigen recognition structures of immunoglobulin and T-cell receptor molecules by combining processes of deletion of terminal coding sequences and addition of nucleotides prior to joining. We have examined the role of coding end DNA composition in junction formation with plasmid substrates containing defined homopolymers flanking the recombination signal sequence elements. We found that coding junctions formed efficiently with or without terminal DNA homology. The extent of junctional deletion was conserved independent of coding ends with increased, partial, or no DNA homology. Interestingly, G/C homopolymer coding ends showed reduced deletion regardless of DNA homology. Therefore, DNA homology cannot be the primary determinant that stabilizes coding end structures for processing and joining.

Animals↗