English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

This report of the general symptoms of blossom-end rot in the tomato describes in detail the anatomical aspects of the disorder. The inception of the rot was observed in field-grown San Marzano tomatoes in relation to the age and development of the fruit. Incipient stages of the rot occurred about 10 to 15 days after anthesis when the fruit was from 38 to 60 per cent full grown in length. During this phase of fruit development the increments of growth in length are very large in relation to the size of the fruit. In general, affected fruits are retarded in length growth. The externally visible and the deep-seated symptoms of the rot may occur separately or together in the same fruit at the distal end. The symptoms involve a progressive necrosis of the tissue with subsequent partial dehydration of the affected area. Variations in the lesions are described. The highest incidence of the rot involved over 55 per cent of the fruit. The first indication of the externally visible lesions is the development of brown proteinaceous inclusions in the epidermal and more deepseated cells of the pericarp. These necrotic cells may collapse and a wound healing response is usually evoked in the adjacent living tissue. Cells showing a wounding response may become necrotic, thus extending the lesion. Light-yellow to brown proteinaceous inclusions also occur in the cells of the deep-seated lesions, particularly in parenchyma cells associated with the vascular bundles of the placental axis. The cells of affected fruits are often glutted with starch grains. No histological evidence was found to support the view that water stress is a primary cause of the disorder. Calcium analysis of the fruit confirms earlier reports that the calcium content of the fruit as a whole is low. The distal end of the fruit, the site of blossom-end rot, is particularly low in calcium. Histological and cytological observations of normal and affected fruits are in agreement with some earlier reports on calcium deficiency in the tomato and other plants. This study implicates calcium deficiency in the fruit as the basic cause of blossom-end rot.

Anatomical aspects of blossom-end rot in the tomato with special reference to calcium nutrition