Chromosome motion during mitosis can be explained by combining the facts available about the equilibrium between the mitotic spindle and its subunits with the postulate that the recently described cross-bridges between spindle microtubules are capable of sliding adjacent tubules over one another.

Model for Mitosis

Using a modified technique which allowed observation of chromosome orientation in the primary oocyte of grasshoppers at the onset of anaphase, it has been possible to establish that the B-chromosome is distributed preferentially on the egg side of the metaphase plate rather than the polar body side. The frequency of this preferential orientation matches very closely the level of preferential transmission determined from breeding experiments using individuals from the same population. The spindle is asymmetrical in the primary oocyte of this species, and a possible explanation of the meiotic drive is proposed as a result of the conical shape of nucleoplasm surrounding this spindle. The autosomal chiasma frequency of these females is generally lower than comparable males and is increased by the presence of B chromosomes; but the chiasma frequencies of the sexes respond differently to the addition of 1 and 2 B-chromosomes.

Meiotic drive for B-chromosomes in the primary oocytes of Myrmeleotettix maculatus (Orthopera: Acrididae).

Two disjunction defective meiotic mutants, ord and mei-S332, each of which disrupts meiosis in both male and female Drosophila melanogaster, were analyzed cytologically and genetically in the male germ-line. It was observed that sister-chromatids are frequently associated abnormally during prophase I and metaphase I in ord. Sister chromatid associations in mei-S332 are generally normal during prophase I and metaphare I. By telophase I, sister chromatids have frequently precociously separated in both mutants. During the first division sister chromatids disjoin from one another frequently in ord and rarely in mei-S332. It is argued that the simplest interpretation of the observations is that each mutant is defective in sister chromatid cohesiveness and that the defect in ord manifests itself earlier than does the defect in mei-S332. In addition, based on these mutant effects, several conclusions regarding normal meiotic processes are drawn. (1) The phenotype of these mutants support the proposition that the second meiotic metaphase (mitotic-type) position of chromosomes and their equational orientation is a consequence of the equilibrium, at the metaphase plate, of pulling forces acting at the kinetochores and directed towards the poles. (2) Chromosomes which lag during the second meiotic division tend to be lost. (3) Sister chromatid cohesiveness, or some function necessary for sister chromatid cohesivenss, is required for the normal reductional orientation of sister kinetochores during the first meiotic division. (4) The kinetochores of a half-bivalent are double at the time of chromosome orientation during the first meiotic division. Finally, functions which are required throughout meiosis in both sexes must be considered in the pathways of meiotic control.

Mechanisms of chromosome orientation revealed by two meiotic mutants in Drosophila melanogaster.

An actin-like component in spermatocytes of a crane fly (Nephrotoma suturalis Loew). I. The spindle.

Decorated actin-like filaments were seen in spindles after crane fly spermatocytes were glycerinated and then treated with rabbit skeletal muscle heavy meromyosin (HMM). Both ATP and pyrophosphate inhibited the HMM reaction. In prometaphase, metaphase, and mid-anaphase cells, actin-like filaments were seen near regions where chromosomal spindle fibres are seen in living cells, and were oriented in the pole-to-pole direction. In the interzone of anaphase cells, actin-like filaments were not oriented in a preferential direction when they were not associated with the microtubules attached to the sex chromosomes. No filaments were seen in glycerinated spindles not treated with HMM. We discuss reasons why filaments might not be seen without prior HMM treatment, and we discuss the possible role of the actin-like filaments in the spindles. — Spindle microtubules often were not seen in cells treated with HMM. This depended on the stage of division: in prometaphase no microtubules were seen; in metaphase microtubules were seen, in apparently normal numbers; in mid-anaphase, microtubules between the autosomes and the poles were seen in reduced numbers, those associated with the equatorial sex-chromosomes were seen in apparently normal numbers, while those between the separating autosomal half-bivalents were not seen. Microtubules were not seen in glycerinated spindles not treated with HMM, suggesting that HMM in some way affects microtubule stability. The question of microtubule stability is briefly discussed.

An actin-like component in sperm tails of a crane fly (Nephrotoma suturalis Loew).

215, 78 (1966). [20] FEOESE, A.: Immunochem. 5, 253 (I968). I21] CHANGEUX, J. P., ef al.: Biochem. 7, 53t (t968). [22] CvERHART, J., u. H. C. SCHAC~MAN: Bioehem. 7, 538 (1968). [23] C~ANGEUX, J. P., u. M.M. RImlN: Biocbem. 7, 553 (~968). [24] WEBER, K.: Nature 218, 1~I6 (1968). [25] KIRSCmVER, t{., e t a h : Prec. Natl. Acad. Sci. (U.S.A.) 56, ~66I ( 1 9 6 6 ) . [26] KIRSCHRE~, K.: Unver6ff. Versuche. [27] JAENICKE, R., u. W. B. GRATZER: Biochemistry (ira Druck). [28] KRATI~Y, O., et aL: Unver/3ff. Versuehe. [29] KIRSCtlNER, K.: Prec. 4. F . E . B. S. Tagung (Osto) I967. Vol. ~. Regulation of Enzyme Activity and Allosterie Interaction. Ed. by E. KVAr~E nnd A. PIHL, p. 39. New York: Academic Press 1968. [30] HESS, B.: Studia Biophysica 2, 41 (1966). [313 HATFIELD, G.W., n. H . E . UMBARGER: Biocbem. Biophys. Res. Comm. 33, 397 (1968). [32] BARBER, t~. D., u. H. J. BRIGHT: Prec. Natl. Aead. Sci. (U.S.A.) 60, 1363 (1968). -[33] GIBSON, Q.H., u. L . J . PARKHURST: J. Biol. Chem. 243, 5521 (1968). [34] SCHUSTER, T. M., u. G. ILGENFRITZ: Nobel Symposium 6: Symmetry and Function of Biological Systems at the MaeromoIeeular Level. Ed. by A. ENGSTR6M und B. STRANDBERG. New York: Interseience Publ. 1969 (ira D r u e k ) . [35] KINGI)ON, H. S., et al.: Biochemistry 7, 2136 (1968).

R. Dietz

Papers

Bau und Funktion des Spindelapparats