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J R Downie

Publications and source records attributed to J R Downie.

7 recordsLinked to original sources
PubMed1988

Scale development in talpid3 mutant chick embryos.

The fact that dermal condensations are not, as they are in feather development, involved in early scale morphogenesis in birds suggests that in the mutant talpid3, where mesenchymal cell surface and motility properties are impaired, scales might develop relatively normally though feathers do not. This prediction has been checked using chorioallantoic membrane grafts of talpid and normal hind limbs, and found to be substantially justified although the abnormal overall shape of the talpid limb has a distorting effect on scale patterning. However, the abnormal talpid dermis seems to have effects on the direction and extent of epidermal invagination at scale margins. Since the control of epidermal invagination is a relatively unexplored area, this is a particularly useful finding.

Animals↗
PubMed1976

The mechanism of chick blastoderm expansion.

At the time of laying, the domestic fowl blastoderm measures 4 mm across. After 4 days' incubation, the extra-embryonic yolk-sac tissues have expanded to encompass the whole yolk mass. This expansion involves the migration over the inner surface of the vitelline membrane of a specialized band of 'edge cells' at the blastoderm periphery. As they move, they pull out the blastoderm behind them, setting up a considerable tension. Expansion also involves cell proliferation and changes in cell shape. This paper attempts to show how locomotion, tension, proliferation and changes in cell shape all contribute to the orderly process of expansion. As a simplification, only the extra-embryonic epiblast is considered here. The findings are: 1. Expansion does not occur at a constant rate, but starts slowly, rises to a peak (over 500 mum/h) at around 3 days, and then slows as coverage of the yolk mass nears completion. 2. During the first day of incubation, edge-cell migration produces a tension in the blastoderm. This rises to peak at 20-24 h, then declines. This tension may be due to an imbalance between expansion by migration and expansion by proliferation. 3. Migration of edge cells can be affected by tension in the blastoderm, i.e. very high tension may hold them back. However, the tension level normally found in the blastoderm seems not to do so. The low rate of expansion in the first day is therefore not due to the high level of tension. It may instead be due to changes in edge-cell organization. 4. Proliferation occurs throughout the extra-embryonic epiblast during the expansion period. It is not restricted to the blastoderm periphery. After the yolk has been covered, the epiblast continues to grow, with proliferation restricted largely to band just distal to the advancing edge of the area vasculosa. 5. Cell shape and arrangement change considerably during expansion. The epiblast of the unincubated embryo is a monolayer of tall cells. During expansion, these become considerably flattened so that each contributes a larger amount to yolk-sac surface area.

Animals↗
PubMed1975

The role of microtubules in chick blastoderm expansion--a quantitative study using colchicine.

Since their discovery, cytoplasmic microtubules have been much studied in the context of cell movement and cell shape change. Much of the work has used drugs, particularly colchicine and its relatives, which break down microtubules- the so-called anti-tubulins. Colchicine and its relatives, which break down microtubules- the so-called anti-tubulins. Colchicine inhibits the orientated movements of many cell types in vitro, and disrupts cell shape change in several morphogenetic situations. The investigatiion reported here used chick blastoderm expansion in New culture in an attempt to quantify the colchicine effect on orientated cell movement. However, although colchicine could halt blastoderm expansion entirely, a simple interpretation was not possible. (1) Colchicine at concentrations capable of blocking mitosis, and of disrupting all or most of the cytoplasmic microtubules of the cells studied, inhibited blastoderm expansion, often resulting in an overall retraction of the cell sheet. (2) Though blastoderm expansion does normally involve considerable cell proliferation, the colchicine effect could not be ascribed to a block on cell division since aminopterin, which stops cell division without affecting microtubules, did not inhibit expansion. (3) Blastoderm expansion is effected by the locomotion of a specialized band of edge cells at the blastoderm periphery. These are the only cells normally attached to the vitelline membrane - the substrate for expansion. When most of the blastoderm was excised, leaving the band of edge cells, and the cultures then treated with colchicine, expansion occurred normally. The colchicine effect on blastoderm expansion could not therefore be ascribed to a direct effect on the edge cells. (4) An alternative site of action of the drug is the remaining cells of the blastoderm. These normally become progressively flatter as expansion proceeds. If flattening in these cells is even partially dependent on their cytoplasmic microtubules, disruption of these microtubules might result in the inherent contractility of the cells resisting and eventually halting edge cell migration. That cell shape in these cells is dependent on microtubules was demonstrated by treating flat blastoderm fragments with colchicine. On incubation, the area occupied by these fragments decreased by 25-30% more than controls. The significance of these results in the general context of orientated cell movements and cell shape determination is discussed, with particular emphasis on the analogous system of Fundulus epiboly.

Aminopterin↗