abstracts of papers presented at the 1962 meetings - Genetics

ABSTRACTS 95 1
An approach to this problem has been made possible in Neurospora by accumulation of markers
induced both in wild-type 74A and other unrelated wild-type strains at the ragged, hist-3,
ad-3A, and nic-2 loci. Crosses involving markers at the ad-3A and nic-2 loci have shown that
a systematic increase in the homogeneity of homologous chromosomes in the ad-3A-nic-2 region
was correlated with a decrease in the frequency of recombination. In other crosses, the lowest
map distances between markers at all four loci were obtained when homologous chromosomes
were derived from the same wild-type strain and the highest map distances when homologs were
of diverse origin. Furthermore, double exchange events in the ragged-hist-3 and hist-3-ad-3A
regions showed negative interference when homologous chromosomes were derived from the
same wild-type strain and positive chromosome interference when of diverse origin. An expla-
nation of these observations in terms of the “effective pairing” concept (R. H. PRITCHARD,
Heredity 9:343, 1955) will be presented.
EBERHART, BRUCE M., P. R. MAHADEVAN, and METTIE B. WHIPPLE, Princeton University,
Princeton, N. J.: Genetic control of the P-glucosidases of Neurospora crassa.-A mutant (gluc-I)
of Neurospora has been obtained that is low in P-glucosidase activity. Three enzymes that attack
p-glucosidic linkages have been compared in gluc-i and wild-type (SY7A) strains. The gluc-1
mutation expresses itself as a reduction in aryl-P-glucosidase, while cellulase and cellobiase are
unaffected by this mutation.-Any attempt to obtain mutations affecting these other enzymes is
made difficult by the overlap in their substrate specificities. The P-glucosidases of Neurospora
have been separated by gradient elution from a DEAE cellulose column. They differ in thermostability,
substrate specificity, affinity for similar substrates, pH optima, and other properties.
Changes in growth conditions cause great changes in the ratios of P-glucosidases in wild-type
mycelia. At temperatures above 30°C cellobiase is greatly reduced. All P-glucosidases are induced
by addition of p-glucosides to the growth media.--Two screening procedures to obtain specific
mutations concerning cellobiase and cellulase have been designed. These procedures (based on the
DE SERRES method) use the optimum growth induction condition for each enzyme in order to
diminish interference by related P-glucosidases.
EDWARDS, JAMES W., and ELDON J. GARDNER, Utah State University, Logan, Utah: Genetic
analysis of a Drosophila melanogaster mutant phenotypically similar to the fourth chromosome
eyeless mutants.-TuRNm and GARDNER (Genetics 45: 915-924) reported the occurrence of flies
with a wide range of morphological abnormalities of the eyes. Because of its phenotypic resemblance
to the fourth chromosome eyeless mutants, the new stock, which was developed by inbreeding,
was designated tentatively as eyeless-prime (&). Genetic analysis has shown that the
major gene associated with the phenotype is located at 97 t 3 crossover units from the left end of
the third chromosome. The new descriptive name eyes-reduced with symbol eyr has been chosen
to replace eyeless-prime. In crosses between eyes-reduced and a wild-type stock, Cockaponsett,
64.8 percent of the F, flies exhibited an eye abnormality. To study the presumed genetic modifiers
of eyr, five homozygous lines were developed using crossover suppressors. These lines possessed
different combinations of eyes-reduced and wild-type chromosomes. By intercrossing,
significant differences were noted with respect to percent of F, flies exhibiting structural eye
abnormalities. Apparently, recessive modifier (s) were carried on the second chromosome of the
eyes-reduced stock. When this stock is homozygous, the F, or heterozygotic expression is decreased.
Preliminary data suggesting a possible interaction between eyes-reduced and ey, eyz, or
ey4 by means of an interaction of modifiers have been obtained. Experiments are being designed
to investigate the action of modifiers in these stocks. (Aided by Damon Runyon Memorial Fund,
Grant DRG-l78F, and by the American Cancer Society, Grant P22-C.)
ERK, FRANK C., and NANCY A. NEVOLE, State University of New York, Long Island Center,
Oyster Bay, N.Y.: The Occurrence of heritable melanotic tumors in Drosophila after larval feeding
OR extracts of tumorous fZies.-When saline extracts of Drosophila melanogaster adults,