The elt-2 Gene and The Regulatory Network Controlling C. elegans Gut Development. Export

@inproceedings{citeulike:3312936, abstract = {How is gut specific gene expression controlled and how is a functioning intestine produced from the single E cell progenitor? The elt-2 gene encodes a single zinc finger GATA transcription factor that is expressed in the gut from the 2E to adult stage. elt-2 is necessary for correct gut cell differentiation, and elt-2 null mutants die at the L1 stage, due to malformed intestines. Although ectopic expression of ELT-2 in the embryo can activate ectopic expression of the gut specific esterase gene (ges-1), gut granules (GG), and a gut specific antigen (MH33), these gut markers are still expressed in the elt-2 mutant. The end-1 gene (described by Rothman lab) also encodes a GATA transcription factor and is expressed in the gut from the 1E to 4E cell stage. Thus, end-1 is a good candidate to compensate for the lack of elt-2. Ectopic expression of end-1 in elt-2 null embryos can indeed activate genes producing MH33 and ICB4 antigens; however, ges-1 is not activated. Thus, some other factor in the early gut of the elt-2 mutant compensates for the lack of elt-2. A possible candidate is a new GATA transcription factor (called elt-4) located 5 kb upstream of elt-2. Elt-2 and elt-4 have highly conserved zinc finger domains as well as N -terminal region. An elt-4 reporter gene construct containing 5 kb of 5' flanking region is expressed in all gut cells as well as 6 cells in the posterior pharynx. We have detected elt-4 mRNA by RT-PCR and are now assembling the entire gene. We will test the function of the elt-4 gene in the gut by using RNAi, ectopic expression experiments and gene knockout. What factors control elt-2 gene expression in the very early gut lineage? We have shown that end-1 can activate elt-2 gene expression through a 700 bp region on the elt-2 promoter. We have also shown that elt-2 autoregulates its own promoter and, by using an in situ GFP assay, have shown that this interaction is direct (See abstract by Fukushige et al.). We are extending our analysis to other genes that may lie upstream of elt-2 as well as to downstream genes that are direct elt-2 targets.}, author = {Fukushige, T. and Mcghee, J. D.}, citeulike-article-id = {3312936}, citeulike-linkout-0 = {http://www.wormbase.org/db/misc/paper?name=WBPaper00023143}, journal = {International C. elegans Meeting}, keywords = {c33d31, c39b106, c\_elegans, caenorhabditis\_elegans, celegans, elegans, elt-2, elt-4, end-1, f58e102, ges-1, meeting\_abstract, nematode, r12a14, wormbase}, posted-at = {2008-09-22 03:16:47}, priority = {3}, title = {The elt-2 Gene and The Regulatory Network Controlling C. elegans Gut Development.}, url = {http://www.wormbase.org/db/misc/paper?name=WBPaper00023143}, year = {1999} }

TY - CONF ID - citeulike:3312936 L3 - citeulike-article-id:3312936 N2 - How is gut specific gene expression controlled and how is a functioning intestine produced from the single E cell progenitor? The elt-2 gene encodes a single zinc finger GATA transcription factor that is expressed in the gut from the 2E to adult stage. elt-2 is necessary for correct gut cell differentiation, and elt-2 null mutants die at the L1 stage, due to malformed intestines. Although ectopic expression of ELT-2 in the embryo can activate ectopic expression of the gut specific esterase gene (ges-1), gut granules (GG), and a gut specific antigen (MH33), these gut markers are still expressed in the elt-2 mutant. The end-1 gene (described by Rothman lab) also encodes a GATA transcription factor and is expressed in the gut from the 1E to 4E cell stage. Thus, end-1 is a good candidate to compensate for the lack of elt-2. Ectopic expression of end-1 in elt-2 null embryos can indeed activate genes producing MH33 and ICB4 antigens; however, ges-1 is not activated. Thus, some other factor in the early gut of the elt-2 mutant compensates for the lack of elt-2. A possible candidate is a new GATA transcription factor (called elt-4) located 5 kb upstream of elt-2. Elt-2 and elt-4 have highly conserved zinc finger domains as well as N -terminal region. An elt-4 reporter gene construct containing 5 kb of 5' flanking region is expressed in all gut cells as well as 6 cells in the posterior pharynx. We have detected elt-4 mRNA by RT-PCR and are now assembling the entire gene. We will test the function of the elt-4 gene in the gut by using RNAi, ectopic expression experiments and gene knockout. What factors control elt-2 gene expression in the very early gut lineage? We have shown that end-1 can activate elt-2 gene expression through a 700 bp region on the elt-2 promoter. We have also shown that elt-2 autoregulates its own promoter and, by using an in situ GFP assay, have shown that this interaction is direct (See abstract by Fukushige et al.). We are extending our analysis to other genes that may lie upstream of elt-2 as well as to downstream genes that are direct elt-2 targets. JF - International C. elegans Meeting TI - The elt-2 Gene and The Regulatory Network Controlling C. elegans Gut Development. KW - c33d31 KW - c39b106 KW - c_elegans KW - caenorhabditis_elegans KW - celegans KW - elegans KW - elt-2 KW - elt-4 KW - end-1 KW - f58e102 KW - ges-1 KW - meeting_abstract KW - nematode KW - r12a14 KW - wormbase AU - Fukushige, T AU - Mcghee, JD PY - 1999/// UR - http://www.wormbase.org/db/misc/paper?name=WBPaper00023143 ER -