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2.
Mol Biol Cell ; 32(4): 331-347, 2021 02 15.
Artículo en Inglés | MEDLINE | ID: mdl-33378215

RESUMEN

Mutations in tubulins affect microtubule (MT) dynamics and functions during neuronal differentiation and their genetic interaction provides insights into the regulation of MT functions. We previously used Caenorhabditis elegans touch receptor neurons to analyze the cellular impact of tubulin mutations and reported the phenotypes of 67 tubulin missense mutations, categorized into three classes: loss-of-function (lf), antimorphic (anti), and neomorphic (neo) alleles. In this study, we isolated 54 additional tubulin alleles through suppressor screens in sensitized backgrounds that caused excessive neurite growth. These alleles included 32 missense mutations not analyzed before, bringing the total number of mutations in our collection to 99. Phenotypic characterization of these newly isolated mutations identified three new types of alleles: partial lf and weak neo alleles of mec-7/ß-tubulin that had subtle effects and strong anti alleles of mec-12/α-tubulin. We also discovered complex genetic interactions among the tubulin mutations, including the suppression of neo mutations by intragenic lf and anti alleles, additive and synthetic effects between mec-7 neo alleles, and unexpected epistasis, in which weaker neo alleles masked the effects of stronger neo alleles in inducing ectopic neurite growth. We also observed balancing between neo and anti alleles, whose respective MT-hyperstablizing and -destabilizing effects neutralized each other.


Asunto(s)
Neuritas/fisiología , Tubulina (Proteína)/genética , Alelos , Secuencia de Aminoácidos , Animales , Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans , Microtúbulos/metabolismo , Microtúbulos/fisiología , Mutación , Mutación Missense , Neuritas/metabolismo , Neurogénesis , Fenotipo , Tubulina (Proteína)/metabolismo
4.
Development ; 147(12)2020 06 17.
Artículo en Inglés | MEDLINE | ID: mdl-32467239

RESUMEN

Molecular chaperones often work collaboratively with the ubiquitylation-proteasome system (UPS) to facilitate the degradation of misfolded proteins, which typically safeguards cellular differentiation and protects cells from stress. In this study, however, we report that the Hsp70/Hsp90 chaperone machinery and an F-box protein, MEC-15, have opposing effects on neuronal differentiation, and that the chaperones negatively regulate neuronal morphogenesis and functions. Using the touch receptor neurons (TRNs) of Caenorhabditis elegans, we find that mec-15(-) mutants display defects in microtubule formation, neurite growth, synaptic development and neuronal functions, and that these defects can be rescued by the loss of Hsp70/Hsp90 chaperones and co-chaperones. MEC-15 probably functions in a Skp-, Cullin- and F-box- containing complex to degrade DLK-1, which is an Hsp90 client protein stabilized by the chaperones. The abundance of DLK-1, and likely other Hsp90 substrates, is fine-tuned by the antagonism between MEC-15 and the chaperones; this antagonism regulates TRN development, as well as synaptic functions of GABAergic motor neurons. Therefore, a balance between the UPS and the chaperones tightly controls neuronal differentiation.


Asunto(s)
Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/metabolismo , Proteínas F-Box/metabolismo , Proteínas HSP90 de Choque Térmico/metabolismo , Microtúbulos/metabolismo , Neuritas/fisiología , Animales , Proteínas de Caenorhabditis elegans/antagonistas & inhibidores , Proteínas de Caenorhabditis elegans/genética , Proteínas F-Box/antagonistas & inhibidores , Proteínas F-Box/genética , Neuronas GABAérgicas/metabolismo , Proteínas HSP90 de Choque Térmico/antagonistas & inhibidores , Proteínas HSP90 de Choque Térmico/genética , Proteínas de Choque Térmico/metabolismo , Quinasas Quinasa Quinasa PAM/metabolismo , Chaperonas Moleculares/antagonistas & inhibidores , Chaperonas Moleculares/genética , Chaperonas Moleculares/metabolismo , Mutagénesis , Neuronas Aferentes/metabolismo , Fosforilación , Complejo de la Endopetidasa Proteasomal/metabolismo , Estabilidad Proteica , Interferencia de ARN , ARN Bicatenario , Ubiquitina/metabolismo , Ubiquitinación
5.
J Neurogenet ; 34(3-4): 247-250, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33446020

RESUMEN

A slide taped to a window at the Woods Hole Marine Biology Laboratory was my first introduction to the touch receptor neurons of the nematode Caenorhabditis elegans. Studying these cells as a postdoc with Sydney Brenner gave me a chance to work with John Sulston on a fascinating set of neurons. I would never have guessed then that 43 years later I would still be excited about learning their secrets.


Asunto(s)
Caenorhabditis elegans/citología , Neurociencias/historia , Células Receptoras Sensoriales/fisiología , Tacto/fisiología , Animales , Caenorhabditis elegans/genética , Caenorhabditis elegans/fisiología , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/fisiología , Dendritas/ultraestructura , Inglaterra , Historia del Siglo XX , Hipoestesia/genética , Hipoestesia/patología , Mecanotransducción Celular/fisiología , Microtúbulos/ultraestructura , Células Receptoras Sensoriales/ultraestructura , Tubulina (Proteína)/genética , Tubulina (Proteína)/fisiología
8.
Development ; 145(22)2018 11 15.
Artículo en Inglés | MEDLINE | ID: mdl-30291162

RESUMEN

Terminal differentiation generates the specialized features and functions that allow postmitotic cells to acquire their distinguishing characteristics. This process is thought to be controlled by transcription factors called 'terminal selectors' that directly activate a set of downstream effector genes. In Caenorhabditis elegans, the differentiation of both the mechanosensory touch receptor neurons (TRNs) and the multidendritic nociceptor FLP neurons uses the terminal selectors UNC-86 and MEC-3. The FLP neurons fail to activate TRN genes, however, because a complex of two transcriptional repressors (EGL-44/EGL-46) prevents their expression. Here, we show that the ZEB family transcriptional factor ZAG-1 promotes TRN differentiation not by activating TRN genes but by preventing the expression of EGL-44/EGL-46. As EGL-44/EGL-46 also inhibits the production of ZAG-1, these proteins form a bistable, negative-feedback loop that regulates the choice between the two neuronal fates.


Asunto(s)
Caenorhabditis elegans/citología , Caenorhabditis elegans/metabolismo , Diferenciación Celular , Linaje de la Célula , Neuronas/citología , Receptores de Superficie Celular/metabolismo , Tacto/fisiología , Animales , Secuencia de Bases , Biomarcadores/metabolismo , Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Regulación del Desarrollo de la Expresión Génica , Modelos Biológicos , Mutación/genética , Neuronas/metabolismo , Penetrancia , Interferencia de ARN , Factores de Tiempo , Factores de Transcripción/metabolismo
9.
J Biol Chem ; 292(38): 15927-15938, 2017 09 22.
Artículo en Inglés | MEDLINE | ID: mdl-28768768

RESUMEN

Paraoxonase-2 (PON-2) is a membrane-bound lactonase with unique anti-oxidative and anti-atherosclerotic properties. PON-2 shares key structural elements with MEC-6, an endoplasmic reticulum-resident molecular chaperone in Caenorhabditis elegans MEC-6 modulates the expression of a mechanotransductive ion channel comprising MEC-4 and MEC-10 in touch-receptor neurons. Because pon-2 mRNA resides in multiple rat nephron segments, including the aldosterone-sensitive distal nephron where the epithelial Na+ channel (ENaC) is expressed, we hypothesized that PON-2 would similarly regulate ENaC expression. We observed PON-2 expression in aquaporin 2-positive principal cells of the distal nephron of adult human kidney. PON-2 also co-immunoprecipitated with ENaC when co-expressed in HEK293 cells. When PON-2 was co-expressed with ENaC in Xenopus oocytes, ENaC activity was reduced, reflecting a reduction in ENaC surface expression. MEC-6 also reduced ENaC activity when co-expressed in Xenopus oocytes. The PON-2 inhibitory effect was ENaC-specific, as PON-2 had no effect on functional expression of the renal outer medullary potassium channel. PON-2 did not alter the response of ENaC to extracellular Na+, mechanical shear stress, or α-chymotrypsin-mediated proteolysis, suggesting that PON-2 did not alter the regulation of ENaC by these factors. Together, our data suggest that PON-2 regulates ENaC activity by modulating its intracellular trafficking and surface expression.


Asunto(s)
Arildialquilfosfatasa/metabolismo , Canales Epiteliales de Sodio/metabolismo , Adulto , Animales , Proteínas de Caenorhabditis elegans/metabolismo , Secuencia Conservada , Canales Epiteliales de Sodio/química , Evolución Molecular , Regulación de la Expresión Génica , Células HEK293 , Humanos , Túbulos Renales Distales/metabolismo , Ratones , Oocitos/metabolismo , Subunidades de Proteína/metabolismo , Ratas
10.
Mol Biol Cell ; 28(21): 2786-2801, 2017 Oct 15.
Artículo en Inglés | MEDLINE | ID: mdl-28835377

RESUMEN

Tubulins, the building block of microtubules (MTs), play a critical role in both supporting and regulating neurite growth. Eukaryotic genomes contain multiple tubulin isotypes, and their missense mutations cause a range of neurodevelopmental defects. Using the Caenorhabditis elegans touch receptor neurons, we analyzed the effects of 67 tubulin missense mutations on neurite growth. Three types of mutations emerged: 1) loss-of-function mutations, which cause mild defects in neurite growth; 2) antimorphic mutations, which map to the GTP binding site and intradimer and interdimer interfaces, significantly reduce MT stability, and cause severe neurite growth defects; and 3) neomorphic mutations, which map to the exterior surface, increase MT stability, and cause ectopic neurite growth. Structure-function analysis reveals a causal relationship between tubulin structure and MT stability. This stability affects neuronal morphogenesis. As part of this analysis, we engineered several disease-associated human tubulin mutations into C. elegans genes and examined their impact on neuronal development at the cellular level. We also discovered an α-tubulin (TBA-7) that appears to destabilize MTs. Loss of TBA-7 led to the formation of hyperstable MTs and the generation of ectopic neurites; the lack of potential sites for polyamination and polyglutamination on TBA-7 may be responsible for this destabilization.


Asunto(s)
Caenorhabditis elegans/crecimiento & desarrollo , Caenorhabditis elegans/metabolismo , Neuritas/metabolismo , Neuritas/fisiología , Tubulina (Proteína)/genética , Tubulina (Proteína)/metabolismo , Secuencia de Aminoácidos , Animales , Proteínas de Caenorhabditis elegans/química , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Humanos , Microtúbulos/genética , Microtúbulos/fisiología , Mutación , Neurogénesis , Neuronas/metabolismo , Isoformas de Proteínas/genética , Tubulina (Proteína)/química
11.
Proc Natl Acad Sci U S A ; 113(25): 6973-8, 2016 06 21.
Artículo en Inglés | MEDLINE | ID: mdl-27274054

RESUMEN

Although previous studies have identified many extracellular guidance molecules and intracellular signaling proteins that regulate axonal outgrowth and extension, most were conducted in the context of unidirectional neurite growth, in which the guidance cues either attract or repel growth cones. Very few studies addressed how intracellular signaling molecules differentially specify bidirectional outgrowth. Here, using the bipolar PLM neurons in Caenorhabditis elegans, we show that the guanine nucleotide exchange factors (GEFs) UNC-73/Trio and TIAM-1 promote anterior and posterior neurite extension, respectively. The Rac subfamily GTPases act downstream of the GEFs; CED-10/Rac1 is activated by TIAM-1, whereas CED-10 and MIG-2/RhoG act redundantly downstream of UNC-73. Moreover, these two pathways antagonize each other and thus regulate the directional bias of neuritogenesis. Our study suggests that directional specificity of neurite extension is conferred through the intracellular activation of distinct GEFs and Rac GTPases.


Asunto(s)
Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/metabolismo , Factores de Intercambio de Guanina Nucleótido/metabolismo , Neuritas/metabolismo , Proteínas de Unión al GTP rac/metabolismo , Animales
12.
G3 (Bethesda) ; 6(4): 1121-30, 2016 04 07.
Artículo en Inglés | MEDLINE | ID: mdl-27172609

RESUMEN

The Caenorhabditis elegans DEG/ENaC proteins MEC-4 and MEC-10 transduce gentle touch in the six touch receptor neurons . Gain-of-function mutations of mec-4 and mec-4(d) result in a hyperactive channel and neurodegeneration in vivo Loss of MEC-6, a putative DEG/ENaC-specific chaperone, and of the similar protein POML-1 suppresses the neurodegeneration caused by a mec-4(d) mutation. We find that mutation of two genes, mec-10 and a new gene mec-19 (previously named C49G9.1), prevents this action of POML-1, allowing the touch receptor neurons to die in poml-1 mec-4(d) animals. The proteins encoded by these genes normally inhibit mec-4(d) neurotoxicity through different mechanisms. MEC-10, a subunit of the mechanosensory transduction channel with MEC-4, inhibits MEC-4(d) activity without affecting MEC-4 expression. In contrast, MEC-19, a membrane protein specific to nematodes, inhibits MEC-4(d) activity and reduces MEC-4 surface expression.


Asunto(s)
Proteínas de Caenorhabditis elegans/genética , Caenorhabditis elegans/fisiología , Canales Epiteliales de Sodio/genética , Proteínas de la Membrana/genética , Secuencia de Aminoácidos , Animales , Animales Modificados Genéticamente , Proteínas de Caenorhabditis elegans/química , Proteínas de Caenorhabditis elegans/metabolismo , Muerte Celular/genética , Canales Epiteliales de Sodio/metabolismo , Regulación de la Expresión Génica , Proteínas de la Membrana/metabolismo , Mutación , Oocitos/metabolismo
14.
Mol Biol Cell ; 27(8): 1272-85, 2016 Apr 15.
Artículo en Inglés | MEDLINE | ID: mdl-26941331

RESUMEN

Caenorhabditis eleganssenses gentle touch via a mechanotransduction channel formed from the DEG/ENaC proteins MEC-4 and MEC-10. An additional protein, the paraoxonase-like protein MEC-6, is essential for transduction, and previous work suggested that MEC-6 was part of the transduction complex. We found that MEC-6 and a similar protein, POML-1, reside primarily in the endoplasmic reticulum and do not colocalize with MEC-4 on the plasma membrane in vivo. As with MEC-6, POML-1 is needed for touch sensitivity, the neurodegeneration caused by themec-4(d)mutation, and the expression and distribution of MEC-4 in vivo. Both proteins are likely needed for the proper folding or assembly of MEC-4 channels in vivo as measured by FRET. MEC-6 detectably increases the rate of MEC-4 accumulation on theXenopusoocyte plasma membrane. These results suggest that MEC-6 and POML-1 interact with MEC-4 to facilitate expression and localization of MEC-4 on the cell surface. Thus MEC-6 and POML-1 act more like chaperones for MEC-4 than channel components.


Asunto(s)
Arildialquilfosfatasa/metabolismo , Proteínas de Caenorhabditis elegans/metabolismo , Proteínas de la Membrana/metabolismo , Animales , Animales Modificados Genéticamente , Arildialquilfosfatasa/genética , Caenorhabditis elegans/genética , Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans/genética , Membrana Celular/metabolismo , Retículo Endoplásmico/metabolismo , Femenino , Transferencia Resonante de Energía de Fluorescencia , Proteínas de la Membrana/genética , Mutación , Neuronas/metabolismo , Neuronas/patología , Oocitos/metabolismo , Xenopus laevis
15.
Curr Top Dev Biol ; 116: 167-80, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-26970619

RESUMEN

Transcription factors control neuronal differentiation by acting as "terminal selectors" that determine the specific cell fates of different types of neurons. The specification of cell fate, however, requires high fidelity, which relies on stable and robust expression of the terminal selectors. Our recent studies in C. elegans suggest that a second set of transcription factors function as reinforcing or protecting factors to stabilize the expression and activity of terminal selectors. Some serve as "guarantors" to ensure the activation and continuous expression of the selectors by reducing stochastic fluctuations in gene expression; others safeguard the protein function of selectors by repressing inhibitors that would block their activity. These transcription factors, unlike the terminal selectors, do not induce specification but secure neuronal cell fate and provide reliability in differentiation.


Asunto(s)
Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/citología , Neuronas/citología , Animales , Caenorhabditis elegans/fisiología , Proteínas de Caenorhabditis elegans/genética , Diferenciación Celular , Regulación del Desarrollo de la Expresión Génica , Proteínas de Homeodominio/genética , Proteínas de Homeodominio/metabolismo , Proteínas con Homeodominio LIM/genética , Proteínas con Homeodominio LIM/metabolismo , Neuronas/fisiología , Proteínas Represoras/genética , Proteínas Represoras/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo
16.
Cell Rep ; 13(7): 1343-1352, 2015 Nov 17.
Artículo en Inglés | MEDLINE | ID: mdl-26547238

RESUMEN

Cell differentiation usually occurs with high fidelity, but the expression of many transcription factors is variable. Using the touch receptor neurons (TRNs) in C. elegans, we found that the Hox proteins CEH-13/lab and EGL-5/Abd-B overcome this variability by facilitating the activation of the common TRN fate determinant mec-3 in the anterior and posterior TRNs, respectively. CEH-13 and EGL-5 increase the probability of mec-3 transcriptional activation by the POU-homeodomain transcription factor UNC-86 using the same Hox/Pbx binding site. Mutation of ceh-13 and egl-5 resulted in an incomplete (∼40%) loss of the TRN fate in respective TRNs, which correlates with quantitative mRNA measurements showing two distinct modes (all or none) of mec-3 transcription. Therefore, Hox proteins act as transcriptional "guarantors" in order to ensure reliable and robust gene expression during terminal neuronal differentiation. Guarantors do not activate gene expression by themselves but promote full activation of target genes regulated by other transcription factors.


Asunto(s)
Proteínas de Caenorhabditis elegans/fisiología , Proteínas de Homeodominio/fisiología , Neurogénesis , Animales , Secuencia de Bases , Sitios de Unión , Caenorhabditis elegans , Regulación del Desarrollo de la Expresión Génica , Neuronas/metabolismo , Regiones Promotoras Genéticas , Transcripción Genética
17.
Neuron ; 88(3): 514-27, 2015 Nov 04.
Artículo en Inglés | MEDLINE | ID: mdl-26539892

RESUMEN

Although Hox genes specify the differentiation of neuronal subtypes along the anterior-posterior axis, their mode of action is not entirely understood. Using two subtypes of the touch receptor neurons (TRNs) in C. elegans, we found that a "posterior induction" mechanism underlies the Hox control of terminal neuronal differentiation. The anterior subtype maintains a default TRN state, whereas the posterior subtype undergoes further morphological and transcriptional specification induced by the posterior Hox proteins, mainly EGL-5/Abd-B. Misexpression of the posterior Hox proteins transformed the anterior TRN subtype toward a posterior identity both morphologically and genetically. The specification of the posterior subtype requires EGL-5-induced repression of TALE cofactors, which antagonize EGL-5 functions, and the activation of rfip-1, a component of recycling endosomes, which mediates Hox activities by promoting subtype-specific neurite outgrowth. Finally, EGL-5 is required for subtype-specific circuit formation by acting in both the sensory neuron and downstream interneuron to promote functional connectivity.


Asunto(s)
Proteínas de Caenorhabditis elegans/genética , Caenorhabditis elegans/crecimiento & desarrollo , Caenorhabditis elegans/genética , Genes Homeobox/genética , Proteínas de Homeodominio/genética , Interneuronas/fisiología , Células Receptoras Sensoriales/fisiología , Factores de Transcripción/genética , Animales , Animales Modificados Genéticamente , Mutación/genética
18.
Proc Natl Acad Sci U S A ; 112(43): 13243-8, 2015 Oct 27.
Artículo en Inglés | MEDLINE | ID: mdl-26460008

RESUMEN

Wnt proteins regulate axonal outgrowth along the anterior-posterior axis, but the intracellular mechanisms that modulate the strength of Wnt signaling in axon guidance are largely unknown. Using the Caenorhabditis elegans mechanosensory PLM neurons, we found that posteriorly enriched LIN-44/Wnt acts as a repellent to promote anteriorly directed neurite outgrowth through the LIN-17/Frizzled receptor, instead of controlling neuronal polarity as previously thought. Dishevelled (Dsh) proteins DSH-1 and MIG-5 redundantly mediate the repulsive activity of the Wnt signals to induce anterior outgrowth, whereas DSH-1 also provides feedback inhibition to attenuate the signaling to allow posterior outgrowth against the Wnt gradient. This inhibitory function of DSH-1, which requires its dishevelled, Egl-10, and pleckstrin (DEP) domain, acts by promoting LIN-17 phosphorylation and is antagonized by planar cell polarity signaling components Van Gogh (VANG-1) and Prickle (PRKL-1). Our results suggest that Dsh proteins both respond to Wnt signals to shape neuronal projections and moderate its activity to fine-tune neuronal morphology.


Asunto(s)
Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/fisiología , Glicoproteínas/metabolismo , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Neuritas/fisiología , Células Receptoras Sensoriales/fisiología , Vía de Señalización Wnt/fisiología , Análisis de Varianza , Animales , Sistemas CRISPR-Cas , Proteínas Dishevelled , Mutagénesis Sitio-Dirigida , Transgenes/genética
19.
Proc Natl Acad Sci U S A ; 112(37): 11690-5, 2015 Sep 15.
Artículo en Inglés | MEDLINE | ID: mdl-26324944

RESUMEN

Caenorhabditis elegans senses gentle touch in the six touch receptor neurons (TRNs) using a mechanotransduction complex that contains the pore-forming degenerin/epithelial sodium channel (DEG/ENaC) proteins MEC-4 and MEC-10. Past work has suggested these proteins interact with the paraoxonase-like MEC-6 and the cholesterol-binding stomatin-like MEC-2 proteins. Using single molecule optical imaging in Xenopus oocytes, we found that MEC-4 forms homotrimers and MEC-4 and MEC-10 form 4:4:10 heterotrimers. MEC-6 and MEC-2 do not associate tightly with these trimers and do not influence trimer stoichiometry, indicating that they are not part of the core channel transduction complex. Consistent with the in vitro data, MEC-10, but not MEC-6, formed puncta in TRN neurites that colocalize with MEC-4 when MEC-4 is overexpressed in the TRNs.


Asunto(s)
Proteínas de Caenorhabditis elegans/fisiología , Caenorhabditis elegans/fisiología , Mecanorreceptores/fisiología , Proteínas de la Membrana/fisiología , Neuronas/fisiología , Animales , Animales Modificados Genéticamente , Arildialquilfosfatasa/química , Proteínas de Caenorhabditis elegans/química , Electrofisiología , Canales Epiteliales de Sodio/química , Mecanotransducción Celular/fisiología , Proteínas de la Membrana/química , Oocitos/citología , Unión Proteica , Multimerización de Proteína , Xenopus laevis
20.
WormBook ; : 1-31, 2015 Jun 18.
Artículo en Inglés | MEDLINE | ID: mdl-26087236

RESUMEN

A little over 50 years ago, Sydney Brenner had the foresight to develop the nematode (round worm) Caenorhabditis elegans as a genetic model for understanding questions of developmental biology and neurobiology. Over time, research on C. elegans has expanded to explore a wealth of diverse areas in modern biology including studies of the basic functions and interactions of eukaryotic cells, host-parasite interactions, and evolution. C. elegans has also become an important organism in which to study processes that go awry in human diseases. This primer introduces the organism and the many features that make it an outstanding experimental system, including its small size, rapid life cycle, transparency, and well-annotated genome. We survey the basic anatomical features, common technical approaches, and important discoveries in C. elegans research. Key to studying C. elegans has been the ability to address biological problems genetically, using both forward and reverse genetics, both at the level of the entire organism and at the level of the single, identified cell. These possibilities make C. elegans useful not only in research laboratories, but also in the classroom where it can be used to excite students who actually can see what is happening inside live cells and tissues.


Asunto(s)
Caenorhabditis elegans/fisiología , Animales , Caenorhabditis elegans/genética , Humanos , Modelos Biológicos
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