Fine Genetic Map of Mouse Chromosome 10 around the Polycystic Kidney Disease Gene,jcpk,and Ankyrin 3

A chlorambucil (CHL)-induced mutation of thejcpk(juvenile congenital polycystic kidney disease) gene causes a severe early onset polycystic kidney disease. In an intercross involvingMus musculus castaneus, jcpkwas precisely mapped 0.2 cM distal toD10Mit115and 0.8 cM proximal toD10Mit173.In addition, five genes,Cdc2a, Col6a1, Col6a2, Bcr,andAnk3were mapped in both thisjcpkintercross and a (BALB/c × CAST/Ei)F₁× BALB/c backcross. All five genes were eliminated as possible candidates forjcpkbased on the mapping data. Thejcpkintercross allowed the orientation of theAnk3gene relative to the centromere to be determined.D10Mit115, D10Mit173, D10Mit199,andD10Mit200were separated genetically in this cross. The order and genetic distances of all markers and gene loci mapped in thejcpkintercross were consistent with those derived from the BALB/c backcross, indicating that the CHL-induced lesion has not generated any gross chromosomal abnormalities detectable in these studies.     

A large-subunit mitochondrial ribosomal DNA sequence translocated to the nuclear genome of two stone crabs (Menippe)

Two DNA sequences that appear to be homologous to large-subunit mitochondrial ribosomal RNA genes have been identified in the stone crabs Menippe mercenaria and M. adina. Amplification from whole genomic DNA by polymerase chain reaction (PCR) with oligonucleotide primers based on conserved portions of large-subunit mitochondrial rRNA genes consistently amplified two products of similar length (565 and 567 bp). These products differed at 3% of their nucleotide bases, and could be distinguished by a HindIII site. Only one of these sequences (designated the A sequence) was detected by PCR in purified mitochondrial DNA. The other (designated the B sequence) hybridized to total genomic DNA at a level consistent with a nuclear genome location. It is unlikely that the type B product would have been recognized as a nuclear copy by examination of its sequence alone. This is the first report of a mitochondrial gene sequence translocated into the nuclear genome of a crustacean.      

H-33-A histocompatibility locus to the left of theH-2 complex

Another minor histocompatibility locus, calledH-33, was found on chromosome 17. This locus was revealed by skin graft experiments between BALB/c and a new congenic strain, BALB.TTF.     

Macrophage-resistant murine simian virus 40 tumors express a retroviral type-specific gp70.

Prototype macrophage-resistant and -sensitive cells were subcloned. Among several subclones of the resistant line, one subclone showed partial reversion to a sensitive phenotype. Analysis with monoclonal antibodies specific for different serotypes of endogenous murine leukemia virus revealed that expression of only one such gp70 (gp70a) correlated with the macrophage-resistant phenotype.     

Extensive deletions in the Q region of the mouse major histocompatibility complex

By use of Southern blot analyses and low copy number probes, the fine structure of the Q region of the mouse major histocompatibility complex was studied in more detail. With a probe recognizing the even-numbered genes Q4, Q6, and Q8, it was evident that Q4 and/or the regions flanking Q4 are polymorphic, whereas Q6 and Q8, and their flanking regions are nonpolymorphic. Perhaps the most noteworthy finding is that at least two strain haplotypes, H-2 ^k and H-2 ^f, possessed extensive deletions in the Q region. The most striking deletion was found in the H-2 ^f haplotype, where the QI through Q9 genes appear to be missing. Because of these extensive deletions the functional importance of the Q region is questioned.     

Desensitization of the human neutrophil degranulation response: Studies with 5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid

The human polymorphonuclear neutrophil degranulation response to 5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid was completely desensitized by preincubating the cells with small amounts of this same fatty acid. Desensitization developed within 1 min, persisted in thoroughly washed cells, and was not due to inactivation of the stimulus. These desensitized cells, however, degranulated partially in response to the ionophore A23187 and normally in response to C5a, N-formyl-methionyl-leucyl-phenylalanine, 1-$\text{0}\text{-}\text{alkyl-2-}\text{0}\text{-}\text{acetyl}\text{-}\text{sn}\text{-}\text{glycero-3-phosphocholine}$, and phorbol myristate acetate. Thus, the dihydroxy fatty acid is a unique stimulus which degranulates and desensitizes neutrophils by pathways at least partially distinct from those utilized by the other stimuli. The fatty acid, although rapidly formed in degranulating neutrophils, is unlikely to be an essential or universal mediator of the degranulation response.