Chordacentrum mineralization is delayed in zebrafish betaglycan‐null mutants

2021 ◽  
Author(s):  
Tonatiuh Molina‐Villa ◽  
Lizbeth Ramírez‐Vidal ◽  
Valentín Mendoza ◽  
Diana Escalante‐Alcalde ◽  
Fernando López‐Casillas
Keyword(s):  
Null Mutants

scholarly journals Caenorhabditis elegans Junctophilin has tissue-specific functions and regulates neurotransmission with extended-synaptotagmin

Genetics ◽  
2021 ◽  
Author(s):  
Christopher A Piggott ◽  
Zilu Wu ◽  
Stephen Nurrish ◽  
Suhong Xu ◽  
Joshua M Kaplan ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Calcium Channel ◽  
Tissue Specific ◽  
Voltage Gated ◽  
Membrane Contact Sites ◽  
Contact Sites ◽  
Pharyngeal Muscles ◽  
Membrane Contact ◽  
Null Mutants

Abstract The junctophilin family of proteins tether together plasma membrane (PM) and endoplasmic reticulum (ER) membranes, and couple PM- and ER-localized calcium channels. Understanding in vivo functions of junctophilins is of great interest for dissecting the physiological roles of ER-PM contact sites. Here, we show that the sole C. elegans junctophilin JPH-1 localizes to discrete membrane contact sites in neurons and muscles and has important tissue-specific functions. jph-1 null mutants display slow growth and development due to weaker contraction of pharyngeal muscles, leading to reduced feeding. In the body wall muscle, JPH-1 co-localizes with the PM-localized EGL-19 voltage-gated calcium channel and ER-localized UNC-68/RyR calcium channel, and is required for animal movement. In neurons, JPH-1 co-localizes with the membrane contact site protein Extended-SYnaptoTagmin 2 (ESYT-2) in soma, and is present near presynaptic release sites. Interestingly, jph-1 and esyt-2 null mutants display mutual suppression in their response to aldicarb, suggesting that JPH-1 and ESYT-2 have antagonistic roles in neuromuscular synaptic transmission. Additionally, we find an unexpected cell non-autonomous effect of jph-1 in axon regrowth after injury. Genetic double mutant analysis suggests that jph-1 functions in overlapping pathways with two PM-localized voltage-gated calcium channels, egl-19 and unc-2, and unc-68/RyR for animal health and development. Finally, we show that jph-1 regulates the colocalization of EGL-19 and UNC-68 and that unc-68/RyR is required for JPH-1 localization to ER-PM puncta. Our data demonstrate important roles for junctophilin in cellular physiology, and also provide insights into how junctophilin functions together with other calcium channels in vivo.

The fluffy Gene of Neurospora crassa Encodes a Gal4p-Type C6 Zinc Cluster Protein Required for Conidial Development

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1813-1820 ◽  
Author(s):  
Lori A Bailey ◽  
Daniel J Ebbole
Keyword(s):  
Transcription Factor ◽  
Neurospora Crassa ◽  
Cosmid Clone ◽  
Developmentally Regulated ◽  
Zinc Cluster ◽  
Conidial Development ◽  
Null Mutants

Abstract Neurospora crassa fluffy (fl) mutants are unable to produce macroconidia. We cloned the fl gene to determine its role in regulating conidiation. A cosmid clone containing fl was identified by complementation. The sequence of fl revealed that it encodes a Gal4p-type C6 zinc cluster protein with greatest similarity to the N. crassa NIT4 protein that regulates genes required for nitrate utilization. Analysis of several fl mutant alleles demonstrated that null mutants are blocked in the budding phase of development required to produce conidiophores. fl mRNA is transiently induced just prior to the developmental commitment to budding growth. This timing of fl expression is consistent with a role for FL protein in activation of the previously characterized conidiation-specific (con) genes, con-6 and con-10. These data suggest that FL acts as a developmentally regulated transcription factor required for conidiophore morphogenesis.

scholarly journals Myosin IB null mutants ofDictyostelium exhibit abnormalities in motility

1991 ◽  
Vol 20 (4) ◽  
pp. 301-315 ◽  
Author(s):  
Deborah Wessels ◽  
John Murray ◽  
Goeh Jung ◽  
John A. Hammer ◽  
David R. Soll
Keyword(s):  
Null Mutants

scholarly journals Comparisons of Mutants Lacking the Golgi UDP-Galactose or GDP-Mannose Transporters Establish that Phosphoglycans Are Important for Promastigote but Not Amastigote Virulence in Leishmania major

2007 ◽  
Vol 75 (9) ◽  
pp. 4629-4637 ◽  
Author(s):  
Althea A. Capul ◽  
Suzanne Hickerson ◽  
Tamara Barron ◽  
Salvatore J. Turco ◽  
Stephen M. Beverley
Keyword(s):  
Golgi Apparatus ◽  
Protective Immunity ◽  
Leishmania Major ◽  
Protozoan Parasite ◽  
Macrophage Infection ◽  
Nucleotide Sugar ◽  
Infectious Cycle ◽  
Null Mutants

ABSTRACT Abundant surface Leishmania phosphoglycans (PGs) containing [Gal(β1,4)Man(α1-PO4)]-derived repeating units are important at several points in the infectious cycle of this protozoan parasite. PG synthesis requires transport of activated nucleotide-sugar precursors from the cytoplasm to the Golgi apparatus. Correspondingly, null mutants of the L. major GDP-mannose transporter LPG2 lack PGs and are severely compromised in macrophage survival and induction of acute pathology in susceptible mice, yet they are able to persist indefinitely and induce protective immunity. However, lpg2 − L. mexicana amastigotes similarly lacking PGs but otherwise normal in known glycoconjugates remain able to induce acute pathology. To explore this further, we tested the infectivity of a new PG-null L. major mutant, which is inactivated in the two UDP-galactose transporter genes LPG5A and LPG5B. Surprisingly this mutant did not recapitulate the phenotype of L. major lpg2 −, instead resembling the L. major lipophosphoglycan-deficient lpg1 − mutant. Metacyclic lpg5A −/lpg5B − promastigotes showed strong defects in the initial steps of macrophage infection and survival. However, after a modest delay, the lpg5A − /lpg5B − mutant induced lesion pathology in infected mice, which thereafter progressed normally. Amastigotes recovered from these lesions were fully infective in mice and in macrophages despite the continued absence of PGs. This suggests that another LPG2-dependent metabolite is responsible for the L. major amastigote virulence defect, although further studies ruled out cytoplasmic mannans. These data thus resolve the distinct phenotypes seen among lpg2 − Leishmania species by emphasizing the role of glycoconjugates other than PGs in amastigote virulence, while providing further support for the role of PGs in metacyclic promastigote virulence.

scholarly journals Hydrogen Peroxide Induces Hyphal Differentiation in Candida albicans

2008 ◽  
Vol 7 (11) ◽  
pp. 2008-2011 ◽  
Author(s):  
Olviyani Nasution ◽  
Kavitha Srinivasa ◽  
Minsun Kim ◽  
Yeo-Jung Kim ◽  
Wankee Kim ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Ascorbic Acid ◽  
Candida Albicans ◽  
Intracellular Concentration ◽  
Low Concentrations ◽  
Null Mutants

ABSTRACT In this study, we demonstrate that hyphal differentiation is induced by the subtoxic concentration of exogenous H2O2 in Candida albicans. This finding is confirmed by the changing intracellular concentration of H2O2. In order to induce the same level of differentiation, low concentrations of exogenous H2O2 are required for the null mutants of the thiol-specific antioxidant and catalase, while higher concentrations are needed for cells treated with ascorbic acid, an antioxidant chemical.

Precocious sporulation and developmental lethality inyelA null mutants ofDictyostelium

1997 ◽  
Vol 20 (4) ◽  
pp. 307-319 ◽  
Author(s):  
Nir Osherov ◽  
Nancy Wang ◽  
William F. Loomis
Keyword(s):  
Null Mutants
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