A conserved Six–Eya cassette acts downstream of Wnt signaling to direct non-myogenic versus myogenic fates in the C. elegans postembryonic mesoderm

Amin, Nirav M.; Lim, Sung-Eun; Shi, Herong; Chan, Tsung-Han; Li, Jun

doi:10.1016/j.ydbio.2009.05.538

Cited by 33 publications

(62 citation statements)

References 68 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3 D and E). A similar expression pattern for a ceh-34::gfp transgene has been independently observed (22). We observed that our ceh-34::gfp transgene was expressed in all pharyngeal neurons (M4, I1, MI, I3, M3, NSM, MC, I2, I4, I5, I6, M1, M2, and M5), some pharyngeal muscle cells (pm1 and pm2) and pharyngeal epithelial cells (e1 and e3), and some body wall muscles around the anterior pharynx (Fig.…”

Section: Ceh-34 Is Expressed Predominantly In the Nuclei Of Pharyngeasupporting

confidence: 73%

See 1 more Smart Citation

Six and Eya promote apoptosis through direct transcriptional activation of the proapoptotic BH3-only geneegl-1inCaenorhabditis elegans

Hirose

Galvin

Horvitz

2010

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The decision of a cell to undergo programmed cell death is tightly regulated during animal development and tissue homeostasis. Here, we show that the Caenorhabditis elegans Six family homeodomain protein C. elegans homeobox (CEH-34) and the Eyes absent ortholog EYA-1 promote the programmed cell death of a specific pharyngeal neuron, the sister of the M4 motor neuron. Loss of either ceh-34 or eya-1 function causes survival of the M4 sister cell, which normally undergoes programmed cell death. CEH-34 physically interacts with the conserved EYA domain of EYA-1 in vitro. We identify an egl-1 5′ cis-regulatory element that controls the programmed cell death of the M4 sister cell and show that CEH-34 binds directly to this site. Expression of the proapoptotic gene egl-1 in the M4 sister cell requires ceh-34 and eya-1 function. We conclude that an evolutionarily conserved complex that includes CEH-34 and EYA-1 directly activates egl-1 expression through a 5′ cis-regulatory element to promote the programmed cell death of the M4 sister cell. We suggest that the regulation of apoptosis by Six and Eya family members is conserved in mammals and involved in human diseases caused by mutations in Six and Eya.cell death | sine oculis | eyes absent | transcription A poptosis, also referred to as programmed cell death, plays fundamental roles in animal development and tissue homeostasis (1). The misregulation of apoptosis is associated with many human disorders, including cancer and neurodegenerative and autoimmune diseases (2). Determining how particular cells are specified to live or die is critical to understanding both normal animal development and human diseases associated with the misregulation of apoptotic cell death.During the development of the Caenorhabditis elegans hermaphrodite, 131 somatic cells undergo programmed cell death (3,4). Genetic studies of programmed cell death in C. elegans have defined an evolutionarily conserved pathway that executes this process (5). This pathway consists of four genes, egl-1 [egg-laying defective (egl)], ced-9 [cell-death abnormal (ced)], ced-4, and ced-3, all of which are conserved from C. elegans to mammals. Although much is understood about the pathway responsible for the execution of programmed cell death in both C. elegans and other animals, less is known about the mechanisms that control how specific cells decide whether to survive or die by programmed cell death. In C. elegans, most of the genes identified to control cell-death specification encode transcription factors, some of which are known to directly regulate the transcription of cell-death genes (6-11). For example, the Snail family transcription factor CES-1 [cell-death specification (ces)] can directly repress expression of the BH3-only proapoptotic gene egl-1 and prevent the deaths of the NSM sister cells (6, 7). This regulatory mechanism is conserved in mammals and has been implicated in human cancer: acute lymphoblastic leukemia results from an overexpression of the CES-1 homolog Slug, which directly represses expre...

show abstract

Section: Ceh-34 Is Expressed Predominantly In the Nuclei Of Pharyngeasupporting

confidence: 73%

“…4B). CEH-34 and EYA-1 also have been shown by others to both act to specify coelomocyte cell fate and interact physically (22).…”

Section: Eya-1 Forms An Evolutionarily Conserved Complex With the Sixmentioning

confidence: 82%

Six and Eya promote apoptosis through direct transcriptional activation of the proapoptotic BH3-only geneegl-1inCaenorhabditis elegans

Hirose

Galvin

Horvitz

2010

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…sem-2(RNAi) construct pCXT9 was made by subcloning the sem-2 cDNA fragment from yk657g12 into L4440 (Timmons and Fire, 1998). pNMA49 and pNMA50 were used for knocking down fozi-1 and mab-5, respectively (Amin et al, 2009).…”

Section: Plasmid Constructs and Transgenic Linesmentioning

confidence: 99%

“…Transgenic lines were generated using the plasmids pRF4 (Mello et al, 1991), pJKL449 (myo-2p::gfp::unc-54 3Ј UTR) (Jiang et al, 2009) or LiuFD61 (mec-7p::mRFP) (Amin et al, 2009) as markers.…”

Section: Plasmid Constructs and Transgenic Linesmentioning

confidence: 99%

“…Water was used as a soaking control. For fozi-1(RNAi) (Amin et al, 2007), let-381(RNAi) (Amin et al, 2010), mab-5(RNAi) and sys-1(RNAi) (Amin et al, 2009) synchronized L1 animals expressing different M lineage markers were plated on HT115(DE3) bacteria expressing dsRNA for the gene of interest. Bacteria for ingestion were prepared as described by Kamath and Ahringer (Kamath and Ahringer, 2003).…”

Section: Rnaimentioning

confidence: 99%

See 1 more Smart Citation

TheC. elegansSoxC protein SEM-2 opposes differentiation factors to promote a proliferative blast cell fate in the postembryonic mesoderm

et al. 2011

Self Cite

View full text Add to dashboard Cite

SUMMARYThe proper development of multicellular organisms requires precise regulation and coordination of cell fate specification, cell proliferation and differentiation. Abnormal regulation and coordination of these processes could lead to disease, including cancer. We have examined the function of the sole C. elegans SoxC protein, SEM-2, in the M lineage, which produces the postembryonic mesoderm. We found that SEM-2/SoxC is both necessary and sufficient to promote a proliferating blast cell fate, the sex myoblast fate, over a differentiated striated bodywall muscle fate. A number of factors control the specific expression of sem-2 in the sex myoblast precursors and their descendants. This includes direct control of sem-2 expression by a Hox-PBC complex. The crucial nature of the HOX/PBC factors in directly enhancing expression of this proliferative factor in the C. elegans M lineage suggests a possible more general link between Hox-PBC factors and SoxC proteins in regulating cell proliferation.

show abstract

Somatic muscle specification during embryonic and post‐embryonic development in the nematode C. elegans

Krause¹,

Li²

2011

WIREs Developmental Biology

Self Cite

View full text Add to dashboard Cite

Myogenesis has proved to be a powerful paradigm for understanding cell fate specification and differentiation in many model organisms. Studies of somatic bodywall muscle (BWM) development in Caenorhabditis elegans allow us to define, with single cell resolution, the distinct hierarchies of transcriptional regulators needed for myogenesis throughout development. Although all 95 BWM cells appear uniform after differentiation, there are several different regulatory cascades employed embryonically and post-embryonically. These, in turn, are integrated into multiple extrinsic cell signaling events. The convergence of these different pathways on the key nodal point, that is the activation of the core muscle module, commits individual cells to myogenesis. Comparisons of myogenesis between C. elegans and other model systems provide insights into the evolution of contractile cell types, demonstrating the conservation of regulatory schemes for muscles throughout the animal kingdom.

show abstract

A conserved Six–Eya cassette acts downstream of Wnt signaling to direct non-myogenic versus myogenic fates in the C. elegans postembryonic mesoderm

Cited by 33 publications

References 68 publications

Six and Eya promote apoptosis through direct transcriptional activation of the proapoptotic BH3-only geneegl-1inCaenorhabditis elegans

Six and Eya promote apoptosis through direct transcriptional activation of the proapoptotic BH3-only geneegl-1inCaenorhabditis elegans

TheC. elegansSoxC protein SEM-2 opposes differentiation factors to promote a proliferative blast cell fate in the postembryonic mesoderm

Somatic muscle specification during embryonic and post‐embryonic development in the nematode C. elegans

Contact Info

Product

Resources

About