Sexual reproduction, a common mode of reproduction among numerous species, involves gametogenesis in which offspring are produced through fertilization, conjugation, or mating. In plants and animals, eggs and sperm differentiate from germ cells to form gametes. However, in budding yeast, spores are produced within diploid cells. During this process, de novo membrane structures form within the cytosol, encapsulating the meiotic haploid nuclei to produce spores. Despite this knowledge, the precise mechanism underlying the formation of these nascent membrane structures remains poorly understood.
To gain insights into this process, researchers at the University of Tsukuba used live imaging techniques to meticulously observe meiosis and sporulation in budding yeast, capturing the development of nascent membrane structures within cells. They observed that although the endoplasmic reticulum (ER) exit sites and Golgi apparatus declined in numbers, they reassembled during sporulation. Furthermore, they identified Gip1, a meiosis-specific subunit of type 1 protein phosphatase, as a key molecule affecting this regulatory mechanism. In Gip1-deficient cells, the secretory pathway could not be precisely located due to the defects in regenerating ER exit sites, resulting in the formation of abnormal spore plasma membranes. This finding suggests that cells efficiently transport membrane lipids and produce new cell membranes by reorganizing membrane traffic pathways during sporulation.
The results of this research have significant implications for human health, as numerous diseases related to gametogenesis and fertilization are caused by abnormalities in intracellular membrane traffic. These findings can potentially enhance the current understanding, diagnosis, and treatment of related pathogenic mechanisms.
This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan (grant numbers 21K06145 to Y.S., 20K05782 and 23K05006 to H.T., 18H05275 to A.N., 22K06074 to K.I.).