The C. elegans Spalt-like protein SEM-4 functions through the SoxC transcription factor SEM-2 to promote a proliferative blast cell fate in the postembryonic mesoderm

• Published in: Developmental biology 2017-09, Vol.429 (1), p.335-342
• Main Authors: Shen, Qinfang, Shi, Herong, Tian, Chenxi, Ghai, Vikas, Liu, Jun
• Format: Article
• Language: English
• Subjects: Animals; Bodywall muscle; Caenorhabditis elegans - cytology; Caenorhabditis elegans - embryology; Caenorhabditis elegans - genetics; Caenorhabditis elegans - metabolism; Caenorhabditis elegans Proteins - metabolism; Cell Differentiation; Cell fate specification; Cell Lineage; Cell Proliferation; Coelomocyte; Differentiation; DNA-Binding Proteins - metabolism; Embryo, Nonmammalian - cytology; Gene Expression Regulation, Developmental; M lineage; Mesoderm; Mesoderm - cytology; Models, Biological; Mutation - genetics; Pluripotent; Proliferation; Regulatory Sequences, Nucleic Acid - genetics; SALL; SEM-2; SEM-4; Sex myoblast; SoxC; SOXC Transcription Factors - metabolism
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2017.06.011

Proper development of a multicellular organism relies on well-coordinated regulation of cell fate specification, cell proliferation and cell differentiation. The C. elegans postembryonic mesoderm provides a useful system for uncovering factors involved in these processes and for further dissecting their regulatory relationships. The single Spalt-like zinc finger containing protein SEM-4/SALL is known to be involved in specifying the proliferative sex myoblast (SM) fate. We have found that SEM-4/SALL is sufficient to promote the SM fate and that it does so in a cell autonomous manner. We further showed that SEM-4/SALL acts through the SoxC transcription factor SEM-2 to promote the SM fate. SEM-2 is known to promote the SM fate by inhibiting the expression of two BWM-specifying transcription factors. In light of recent findings in mammals showing that Sall4, one of the mammalian homologs of SEM-4, contributes to pluripotency regulation by inhibiting differentiation, our work suggests that the function of SEM-4/SALL proteins in regulating pluripotency versus differentiation appears to be evolutionarily conserved. •SEM-4 is necessary and sufficient to specify the multipotent sex myoblast (SM) fate.•sem-4 functions autonomously to specify the SM fate.•SEM-4 functions through the SoxC transcription factor SEM-2 to specify the SM fate.