Cell-lineage and developmental defects of temperature-sensitive embryonic arrest mutants of the nematodeCaenorhabditis elegans

1984 ◽  
Vol 193 (3) ◽  
pp. 164-179 ◽  
Author(s):  
Kenneth T. R. Denich ◽  
Einhard Schierenberg ◽  
Edoardo Isnenghi ◽  
Randall Cassada
Keyword(s):  
Cell Lineage ◽  
Temperature Sensitive ◽  
Developmental Defects ◽  
Embryonic Arrest

METTL3-mediated m6A methylation negatively modulates autophagy to support blastocyst development

2020 ◽  
Author(s):  
Zubing Cao ◽  
Ling Zhang ◽  
Renyun Hong ◽  
Yiqing Wang ◽  
Xin Qi ◽  
...  
Keyword(s):  
Single Cell Analysis ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Blastocyst Development ◽  
Developmental Defects ◽  
Trophectoderm Cells ◽  
Early Embryos ◽  
Embryonic Arrest ◽  
Autophagy Activity ◽  
Inhibitor Treatment

Abstract Background: N6-methyladenosine (m6A) catalyzed by METTL3 regulates the maternal-to-zygotic transition in zebrafish and mice. However, the role and mechanism of METTL3-mediated m6A methylation in blastocyst development remains unclear. Results: We found that reduced m6A levels triggered by METTL3 knockdown caused embryonic arrest during morula-blastocyst transition and developmental defects in trophectoderm cells. Intriguingly, overexpression of METTL3 in early embryos resulted in increased m6A levels and these embryos phenocopied METTL3 knockdown embryos. Mechanistically, METTL3 knockdown or overexpression resulted in a significant increase or decrease in expression of ATG5 and LC3 (an autophagy marker) in blastocysts, respectively. m6A modification of ATG5 mRNA mainly occurs at 3’UTR, and METTL3 knockdown enhanced ATG5 mRNA stability, suggesting that METTL3 negatively regulated autophagy in an m6A dependent manner. Furthermore, single-cell analysis revealed that METTL3 knockdown only increased expression of LC3 and ATG5 in trophectoderm cells, indicating preferential inhibitory effects of METTL3 on autophagy activity in the trophectoderm lineage. Importantly, autophagy restoration by 3MA (an autophagy inhibitor) treatment partially rescued developmental defects of METTL3 knockdown blastocysts. Conclusions: Our results demonstrate that METTL3-mediated m6A methylation negatively modulates autophagy to support blastocyst development.

Temperature-sensitive mutations that arrest Arabidopsis shoot development

Development ◽  
1996 ◽  
Vol 122 (12) ◽  
pp. 3799-3807 ◽  
Author(s):  
F.B. Pickett ◽  
M.M. Champagne ◽  
D.R. Meeks-Wagner
Keyword(s):  
Apical Meristem ◽  
Shoot Development ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
Normal Leaf ◽  
Temperature Dependent ◽  
Leaf Morphogenesis ◽  
Developmental Defects ◽  
Leaf Initiation ◽  
Reduced Rate

To identify genes involved in meristem function we have designed a screen for temperature-sensitive mutations that cause a conditional arrest of early shoot development in Arabidopsis. We describe the characterization of three mutations, arrested development (add) 1, 2 and 3. At the restrictive temperature the add1 and add2 mutations disrupt apical meristem function as assayed by leaf initiation. Furthermore, add1 and add2 plants exhibit defects in leaf morphogenesis following upshift from permissive to restrictive temperature. This result suggests that proximity to a functional meristem is required for the completion of normal leaf morphogenesis. The add3 mutation does not have a dramatic effect on the production of leaves by the apical meristem; however, add3 prevents the expansion of leaf blades at high temperature. Thus, in this mutant the temperature-dependent arrest of epicotyl development is due to a failure of normal leaf development rather than new leaf initiation. While all add mutants have a reduced rate of root growth in comparison to wild-type plants, the mutants do not display a temperature-dependent arrest of root development. All add mutants display some developmental defects at low temperature, suggesting that these mutations affect genes involved in inherently temperature-sensitive developmental processes.

scholarly journals Dissecting gonadal cell lineage specification and sex determination during human development using a single-cell transcriptomics approach

2020 ◽  
Author(s):  
Fuchou Tang ◽  
Rui Wang ◽  
Xixi Liu ◽  
Li Li ◽  
Ming Yang ◽  
...  
Keyword(s):  
Sex Determination ◽  
Sertoli Cells ◽  
Leydig Cells ◽  
Receptor Gene ◽  
Somatic Cells ◽  
Gonad Development ◽  
Cell Lineage ◽  
Human Embryos ◽  
Developmental Defects ◽  
Steroidogenic Cell

Abstract Gonadal somatic cells are the main players in gonad development and are important for sex determination and germ cell development. Here, using a time-series scRNA-seq strategy, we analyzed the fetal germ cells (FGCs) and gonadal somatic cells in human embryos and fetuses. Clustering analysis of testes and ovaries revealed several novel cell subsets, including POU5F1+SPARC+ FGCs and KRT19+ somatic cells. Furthermore, our data indicated that DLK1+ cells may be the progenitors of steroidogenic cell lineages in both sexes and that TAC1+ cells may be the progenitors of granulosa cells in females. Intriguingly, the testosterone synthesis function transitioned from fetal Sertoli cells to adult Leydig cells in a step-wise manner. Moreover, interactions between gonadal somatic cells were systematically explored and verified in our study. In detail, we observed that Sertoli cells interacted with Leydig cells through DHH-PTCH1 and PDGFA-PDGFRA/PDGFRB ligand-receptor gene pairs. More importantly, we identified cell type-specific developmental defects of both FGCs and gonadal somatic cells in a Turner syndrome embryo (45, XO). Our work provides a blueprint of the complex yet highly ordered development and interactions of human FGCs and gonadal microenvironment cells.

Conditional absence of mitosis-specific antigens in a temperature-sensitive embryonic-arrest mutant of Caenorhabditis elegans

1987 ◽  
Vol 87 (2) ◽  
pp. 305-314 ◽  
Author(s):  
R.M. Hecht ◽  
M. Berg-Zabelshansky ◽  
P.N. Rao ◽  
F.M. Davis
Keyword(s):  
Caenorhabditis Elegans ◽  
Mammalian Cells ◽  
Temperature Shift ◽  
Temperature Sensitive ◽  
Restrictive Temperature ◽  
C Elegans ◽  
Phosphatase Treatment ◽  
M Phase ◽  
A Cell ◽  
Embryonic Arrest

A monoclonal antibody, specific to phosphoproteins in mitotic HeLa cells was found to crossreact with a similar set of proteins in embryos of the nematode, Caenorhabditis elegans. In C. elegans, as in mammalian cells, the highly conserved antigenic epitope is associated with a family of high molecular weight polypeptides. The antigenic reactivity of these multiple proteins also depends on their phosphorylation, since antibody binding is reduced after alkaline phosphatase treatment. The antigens are detected at the centrosomes, and in the nuclear region and surrounding cytoplasm of mitotic cells. The significance of these antigens is emphasized by their absence at restrictive temperature in embryos of the temperature-sensitive embryonic-arrest mutant, emb-29V. Furthermore, temperature shift-down experiments suggest that the emb-29 mutation defines a cell division cycle function that affects an essential activity required for progression into M phase.

TEMPERATURE-DEPENDENT EXPRESSION OF THE APTEROUS PHENOTYPE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 217-228
Author(s):  
Mary E Stevens ◽  
Peter J Bryant
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Gene Product ◽  
Constant Temperature ◽  
Temperature Shift ◽  
Sensitive Period ◽  
Temperature Sensitive ◽  
Temperature Dependent ◽  
Developmental Defects ◽  
Per Se

ABSTRACT Mutations at the apterous (ap) locus in Drosophila melanogaster produce a variety of developmental defects, including several classes of wing abnormalities. We describe the wing phenotype produced by homozygotes and hemizygotes of three different temperature-sensitive apterous alleles grown at 16, 18, 20, 22, 25, and 29°. We also describe the phenotype produced by each of these three alleles when heteroallelic with the non-temperature-sensitive apc allele. Constant-temperature and temperature-shift experiments show that each of the heteroallelic genotypes can produce several of the previously described apterous phenotypes and that the length of the temperature-sensitive period for a given phenotype depends on the allelic combinations used to measure it. We suggest that the stage-specific requirements of the tissue for gene product, rather than the time of gene expression per se, determine the temperature-sensitive periods for apterous and other loci. The results support the hypothesis that the various wing phenotypes produced by apterous mutations are due to quantitative reductions in the activity of gene product and that failure to meet specific threshold requirements for gene product can lead to qualitatively different phenotypes.

gon-2, a Gene Required for Gonadogenesis in Caenorhabditis elegans

Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1077-1089 ◽  
Author(s):  
Andrew Y Sun ◽  
Eric J Lambie
Keyword(s):  
Caenorhabditis Elegans ◽  
Larval Stage ◽  
Cell Lineage ◽  
Temperature Sensitive ◽  
Loss Of Function ◽  
Primary Defect ◽  
Cell Fates ◽  
Fourth Larval Stage ◽  
Full Complement ◽  
Sensitive Allele

The gonad of the Caenorhabditis elegans hermaphrodite is generated by the postembryonic divisions of two somatic precursors, Z1 and Z4, and two germline precursors, Z2 and Z3. These cells begin division midway through the first larval stage. By the end of the fourth larval stage, Z1 and Z4 produce 143 descendants, while Z2 and Z3 give rise to ∼1000 descendants. The divisions of Z2 and Z3 are dependent on signals produced by Z1 and Z4, but not vice versa. We have characterized the properties of five loss-of-function alleles of a newly described gene, which we call gon-2. In gon-2 mutants, gonadogenesis is severely impaired; in some animals, none of the gonad progenitors undergo any postembryonic divisions. Mutations in gon-2 have a partial maternal effect: either maternal or zygotic expression is sufficient to prevent the severe gonadogenesis defects. By cell lineage analysis, we found that the primary defect in gon-2 mutants is a delay (sometimes a complete block) in the onset and continuation of gonadal divisions. The results of upshift experiments using a temperature-sensitive allele suggest that zygotic expression of gon-2 begins early in embryogenesis, before the birth of Z1 and Z4. The results of downshift experiments suggest that Z1 and Z4 can generate the full complement of gonadal tissues even when gon-2 function is inhibited until the end of the second larval stage. Thus, gon-2 activity is probably not required for the specification of gonadal cell fates, but appears to be generally required for gonadal cell divisions.

scholarly journals Rac GTPase isoforms Rac1 and Rac2 play a redundant and crucial role in T-cell development

Blood ◽  
2008 ◽  
Vol 112 (5) ◽  
pp. 1767-1775 ◽  
Author(s):  
Fukun Guo ◽  
Jose A. Cancelas ◽  
David Hildeman ◽  
David A. Williams ◽  
Yi Zheng
Keyword(s):  
T Cell ◽  
T Cell Development ◽  
Cell Lineage ◽  
Cell Receptor ◽  
Cell Development ◽  
Rac Gtpase ◽  
Developmental Defects ◽  
Hematopoietic Stem ◽  
And Migration ◽  
Specific Deletion

Abstract Rac GTPases have been implicated in the regulation of diverse functions in various blood cell lineages, but their role in T-cell development is not well understood. We have carried out conditional gene targeting to achieve hematopoietic stem cell (HSC)– or T-cell lineage–specific deletion of Rac1 or Rac1/Rac2 by crossbreeding the Mx-Cre or Lck-Cre transgenic mice with Rac1loxp/loxp or Rac1loxp/loxp;Rac2−/− mice. We found that (1) HSC deletion of both Rac1 and Rac2 inhibited production of common lymphoid progenitors (CLPs) in bone marrow and suppressed T-cell development in thymus and peripheral organs, whereas deletion of Rac1 moderately affected CLP production and T-cell development. (2) T cell–specific deletion of Rac1 did not affect T-cell development, whereas deletion of both Rac1 and Rac2 reduced immature CD4+CD8+ and mature CD4+ populations in thymus as well as CD4+ and CD8+ populations in spleen. (3) The developmental defects of Rac1/Rac2 knockout T cells were associated with proliferation, survival, adhesion, and migration defects. (4) Rac1/Rac2 deletion suppressed T-cell receptor–mediated proliferation, IL-2 production, and Akt activation in thymocytes. Thus, Rac1 and Rac2 have unique roles in CLP production and share a redundant but essential role in later stages of T-cell development by regulating survival and proliferation signals.

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