Abstract

Pumpkin seeds are used globally for snacks, bakery, and oil due to their nutritional and medicinal properties. The seeds of pumpkin have 35–45% oil, rich in health-enhancing fatty acids especially linoleic (52.7%), oleic (28.3%), and palmitic (12.7%). However, the presence of thick leathery seed coat (hull) limits the use due to decortication process required for further use. A mutant carrying thin and papery layer overcame the barrier of cost, time, and labor for decortication of pumpkin seed. The recessive gene mutation prevents lignin deposition and leads to collapse of the middle testa layers of the pumpkin seed. Mutation also changed the color of seeds from white to olive-green and produced dark-colored oil. Seed testa remains the same as in wild variety with five distinct testa layers of epidermis (E), hypodermis (H), sclerenchyma (S), parenchyma (P), and innermost chlorenchyma (C) during the initial stages of development. The changes in the seed testa start with the lignification process, which coincides with the reduced polyamine content. Lignin deposition diminution also coincides with reduced expression of the genes or enzyme activities involved in secondary wall formation. This suggests that, the mutation led to a series of changes to bring about a single response, i.e., naked seed or hull-less seed. Thus, this mutation should be studied thoroughly to determine the effects causing reduced lignin deposition and production of hull-less seeds. This review is focused on the changes induced by mutation that causes hull-less seed trait and its implications for commercial use.

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