scholarly journals The Heterochronic Gene lin-14 Controls Axonal Degeneration in C. elegans Neurons

Cell Reports ◽  
2017 ◽  
Vol 20 (12) ◽  
pp. 2955-2965 ◽  
Author(s):  
Fiona K. Ritchie ◽  
Rhianna Knable ◽  
Justin Chaplin ◽  
Rhiannon Gursanscky ◽  
Maria Gallegos ◽  
...  
Keyword(s):  
Axonal Degeneration ◽  
C Elegans ◽  
Heterochronic Gene

scholarly journals Novel gain-of-function alleles demonstrate a role for the heterochronic gene lin-41 in C. elegans male tail tip morphogenesis

2006 ◽  
Vol 297 (1) ◽  
pp. 74-86 ◽  
Author(s):  
Tania Del Rio-Albrechtsen ◽  
Karin Kiontke ◽  
Shu-Yi Chiou ◽  
David H.A. Fitch
Keyword(s):  
Gain Of Function ◽  
Male Tail ◽  
C Elegans ◽  
Heterochronic Gene ◽  
Tail Tip

scholarly journals The Apoptotic Engulfment Machinery Regulates Axonal Degeneration in C. elegans Neurons

Cell Reports ◽  
2016 ◽  
Vol 14 (7) ◽  
pp. 1673-1683 ◽  
Author(s):  
Annika L.A. Nichols ◽  
Ellen Meelkop ◽  
Casey Linton ◽  
Rosina Giordano-Santini ◽  
Robert K. Sullivan ◽  
...  
Keyword(s):  
Axonal Degeneration ◽  
C Elegans

scholarly journals A cohort of Caenorhabditis species lacking the highly conserved let-7 microRNA

2020 ◽  
Author(s):  
Charles Nelson ◽  
Victor Ambros
Keyword(s):  
Cell Fate ◽  
Nematode Species ◽  
Loss Of Function ◽  
Animal Development ◽  
C Elegans ◽  
Adult Transition ◽  
Developmental Progression ◽  
Caenorhabditis Species ◽  
Heterochronic Gene ◽  
Bilaterian Animal

ABSTRACTlet-7 is a highly conserved microRNA with critical functions integral to cell fate specification and developmental progression in diverse animals. In Caenorhabditis elegans, let-7 is a component of the heterochronic (developmental timing) gene regulatory network, and loss-of-function mutations of let-7 result in lethality during the larval to adult transition due to misregulation of the conserved let-7 target, lin-41. To date, no bilaterian animal lacking let-7 has been characterized. In this study, we identify a cohort of nematode species within the genus Caenorhabditis, closely related to C. elegans, that lack the let-7 microRNA, owing to absence of the let-7 gene. Using C. sulstoni as a representative let-7-lacking species to characterize normal larval development in the absence of let-7, we demonstrate that, except for the lack of let-7, the heterochronic gene network is otherwise functionally conserved. We also report that species lacking let-7 contain a group of divergent let-7 orthologs -- also known as the let-7-family of microRNAs -- that have apparently assumed the role of targeting the lin-41 mRNA.Summary StatementWe have identified a group of Caenorhabditis species that lack let-7a, an otherwise highly conserved and nearly ubiquitous microRNA that was previously thought to be critical to bilaterian animal development.

scholarly journals The C. elegans heterochronic gene lin-28 coordinates the timing of hypodermal and somatic gonadal programs for hermaphrodite reproductive system morphogenesis

2018 ◽  
Author(s):  
Sungwook Choi ◽  
Victor Ambros
Keyword(s):  
Control Cell ◽  
Gonad Development ◽  
Developmental Timing ◽  
Specific Cell ◽  
Cell Fates ◽  
C Elegans ◽  
Gonad Morphology ◽  
Somatic Gonad ◽  
Heterochronic Gene ◽  
A Cell

AbstractC. elegans heterochronic genes determine the timing of expression of specific cell fates in particular stages of developing larva. However, their broader roles in coordinating developmental events across diverse tissues has been less well investigated. Here, we show that loss of lin-28, a central heterochronic regulator of hypodermal development, causes reduced fertility associated with abnormal somatic gonad morphology. In particular, the abnormal spermatheca-uterine valve morphology of lin-28(lf) hermaphrodites trap embryos in the spermatheca, which disrupts ovulation and causes embryonic lethality. The same genes that act downstream of lin-28 in the regulation of hypodermal developmental timing also act downstream of lin-28 in somatic gonad morphogenesis and fertility. Importantly, we find that hypodermal expression, but not somatic gonadal expression, of lin-28 is sufficient for restoring normal somatic gonad morphology in lin-28(lf) mutants. We propose that the abnormal somatic gonad morphogenesis of lin-28(lf) hermaphrodites results from temporal discoordination between the accelerated hypodermal development and normally timed somatic gonad development. Thus, our findings exemplify how a cell-intrinsic developmental timing program can also control cell non-autonomous signaling critical for proper development of other interacting tissues.

scholarly journals A cohort of Caenorhabditis species lacking the highly conserved let-7 microRNA

2021 ◽  
Author(s):  
Charles Nelson ◽  
Victor Ambros
Keyword(s):  
Cell Fate ◽  
Nematode Species ◽  
Loss Of Function ◽  
C Elegans ◽  
Adult Transition ◽  
Developmental Progression ◽  
Caenorhabditis Species ◽  
Heterochronic Gene ◽  
Bilaterian Animal

Abstract The let-7 gene encodes a highly conserved microRNA with critical functions integral to cell fate specification and developmental progression in diverse animals. In Caenorhabditis elegans, let-7 is a component of the heterochronic (developmental timing) gene regulatory network, and loss-of-function mutations of let-7 result in lethality during the larval to adult transition due to misregulation of the conserved let-7 target, lin-41. To date, no bilaterian animal lacking let-7 has been characterized. In this study, we identify a cohort of nematode species within the genus Caenorhabditis, closely related to C. elegans, that lack the let-7 microRNA, owing to absence of the let-7 gene. Using C. sulstoni as a representative let-7-lacking species to characterize normal larval development in the absence of let-7, we demonstrate that, except for the lack of let-7, the heterochronic gene network is otherwise functionally conserved. We also report that species lacking let-7 contain a group of divergent let-7 paralogs—also known as the let-7-family of microRNAs—that have apparently assumed the role of targeting the lin-41 mRNA.

Mechanisms of Axonal Degeneration and Regeneration

2017 ◽  
pp. 574-592 ◽  
Author(s):  
Jiaxing Li ◽  
Catherine A. Collins
Keyword(s):  
Axonal Degeneration ◽  
Morphological Changes ◽  
Axonal Injury ◽  
Model Organisms ◽  
C Elegans ◽  
The Face ◽  
Invertebrate Model ◽  
Critical Components ◽  
Injury Models ◽  
Shed Light

In the face of acute or chronic axonal damage, neurons and their axons undergo a number of molecular, cellular, and morphological changes. These changes facilitate two types of responses, axonal degeneration and regeneration, both of which are remarkably conserved in both vertebrates and invertebrates. Invertebrate model organisms, including Drosophila and C. elegans, have offered a powerful platform with accessible genetic tools for manipulation and amenable nervous system for visualization. Thus far, several critical components and pathways in axonal degeneration and regeneration have been identified in invertebrate studies, including Sarm and Wallenda/DLK. This article highlights important findings in Drosophila, C. elegans, and other invertebrate injury models that have shed light upon the mechanism in axonal injury response.

scholarly journals Molecular genetics of the Caenorhabditis elegans heterochronic gene lin-14.

Genetics ◽  
1989 ◽  
Vol 121 (3) ◽  
pp. 501-516 ◽  
Author(s):  
G Ruvkun ◽  
V Ambros ◽  
A Coulson ◽  
R Waterston ◽  
J Sulston ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Yeast Artificial Chromosome ◽  
Artificial Chromosome ◽  
General Strategy ◽  
Cis Acting ◽  
Temporal Regulation ◽  
C Elegans ◽  
Dna Alterations ◽  
Heterochronic Gene ◽  
Systematic Identification

Abstract We describe a general strategy for the genetic mapping in parallel of multiple restriction fragment length polymorphism (RFLP) loci. This approach allows the systematic identification for cloning of physical genetic loci within about 100 kb of any gene in Caenorhabditis elegans. We have used this strategy of parallel RFLP mapping to clone the heterochronic gene lin-14, which controls the timing and sequence of many C. elegans postembryonic developmental events. We found that of about 400 polymorphic loci in the C. elegans genome associated with the Tc1 family of repetitive elements, six are within 0.3 map unit of lin-14. The three closest lin-14-linked Tc1-containing restriction fragments were cloned and used to identify by hybridization an 830-kb region of contiguous cloned DNA fragments assembled from cosmid and yeast artificial chromosome libraries. A lin-14 intragenic recombinant that separated a previously cryptic lin-14 semidominant mutation from a cis-acting lin-14 suppressor mutation was used to map the location of the lin-14 gene to a 25-kb region of this 830-kb contig. DNA probes from this region detected lin-14 allele-specific DNA alterations and a lin-14 mRNA. Two lin-14 semi-dominant alleles, which cause temporally inappropriate lin-14 gene activity and lead to the reiterated expression of specific early developmental events, were shown to delete sequences from the lin-14 gene and mRNA. These deletions may define cis-acting sequences responsible for the temporal regulation of lin-14.

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