{"id":1632,"date":"2020-03-10T16:55:55","date_gmt":"2020-03-10T08:55:55","guid":{"rendered":"http:\/\/www.bioactivescreeninglibrary.com\/?p=1632"},"modified":"2022-01-07T10:56:45","modified_gmt":"2022-01-07T02:56:45","slug":"genes-function-signaling-intestinal-cells-regulate-properties","status":"publish","type":"post","link":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/2020\/03\/10\/genes-function-signaling-intestinal-cells-regulate-properties\/","title":{"rendered":"The same genes that function during signaling to specify to make intestinal cells also regulate several other properties"},"content":{"rendered":"

Racteristics of the E lineage are tightly associated with the ability of E to generate differentiated intestinal cells. In mutant embryos that fail to make intestinal cells, E daughters tend to divide earlier than E daughters in wildtype embryos, and they do not initiate gastrulation. In embryos mutant for skn-1, med-1\/2, and\/or end-1\/3, if intestinal cells are produced, their number is usually abnormal. In embryos carrying a loss-of-function mutation in cki-1, a negative regulator of cell cycle progression, or a gain-of-function mutation in cdc-25, a positive regulator, the E lineage undergoes one extra round of cell division. When either of these mutations is combined with a mutation where the E blastomere adopts the fate of MS, the transformed E blastomere undergoes the number of cell divisions and with cell cycle timing typical for a wildtype MS blastomere. The above observations suggest that the (+)-JQ1 Epigenetic Reader Domain inhibitor<\/a> P2-EMS signal at the 4cell stage leads to the many different characteristics of the E lineage, in addition to intestinal development. We know very little about how these characteristics of E lineage fate, other than intestinal differentiation, is regulated by the P2-EMS signal. The P2-EMS interaction could lead to the direct activation of a master gene, which then regulates a number of downstream target genes, resulting in the generation of the complete E phenotype as outlined above. Alternatively, the P2-EMS signals could result in the direct activation of a suite of genes, each of which regulates separate pathways that together lead to the full E lineage phenotype. We and others have identified, through molecular approaches, several zygotically-expressed genes whose restricted or highly-enriched expression in the E blastomere is dependent on the same set of genes that specify E as the intestinal precursor. This includes sdz-23, which encodes a protein with an EGF-like motif, and sdz-26, which encodes an F-box containing protein. Neither of these genes appears to have a function in the specification of E as an intestinal precursor or in the differentiation of intestinal cells. In fact, no specific function has yet been ascribed to either gene. Identification of these zygotic genes expressed early in the E lineage suggests that the P2-EMS interaction has molecular consequences beyond specifying E as the endoderm precursor. Here, we show that the different characteristics of the E lineage fate can be uncoupled in certain mutants. Many embryos carrying mutations for P2-EMS signaling genes can generate an intestinal cell lineage which loses count of the normal number of cell divisions. Mutation in the cell cycle regulator wee-1.1 results in a shortened cell cycle for E daughters Ea and Ep, without affecting intestinal differentiation or embryogenesis, and these worms are viable. In addition, expression of three E-specific genes, assayed in individual embryos mutant for P2-EMS signaling components, are affected discordantly and stochastically. Our results support the model whereby certain aspects of the E lineage program are independently regulated by the P2-EMS signaling. An E blastomere isolated from an 8-cell embryo exhibits many properties of the E lineage in an intact embryo.<\/p>\n","protected":false},"excerpt":{"rendered":"

Racteristics of the E lineage are tightly associated with the ability of E to generate differentiated intestinal cells. In mutant embryos that fail to make intestinal cells, E daughters tend to divide earlier than E daughters in wildtype embryos, and they do not initiate gastrulation. In embryos mutant for skn-1, med-1\/2, and\/or end-1\/3, if intestinal … Continue reading “The same genes that function during signaling to specify to make intestinal cells also regulate several other properties”<\/span><\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[1],"tags":[],"_links":{"self":[{"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/posts\/1632"}],"collection":[{"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/comments?post=1632"}],"version-history":[{"count":1,"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/posts\/1632\/revisions"}],"predecessor-version":[{"id":1633,"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/posts\/1632\/revisions\/1633"}],"wp:attachment":[{"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/media?parent=1632"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/categories?post=1632"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/www.bioactivescreeninglibrary.com\/index.php\/wp-json\/wp\/v2\/tags?post=1632"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}