Summary
Members of the Fusarium solani species complex (FSSC) are capable of causing disease in many agriculturally important crops The genomes of some of these fungi include supernumerary chromosomes that are dispensable and encode host-specific virulence factors In addition to genomics, this review summarizes the known molecular mechanisms utilized by members of the FSSC in establishing disease

Taxonomy
Kingdom Fungi; Phylum Ascomycota; Class Sordariomycetes; Order Hypocreales; Family Nectriaceae; Genus Fusarium

Host range
Members of the FSSC collectively have a very broad host range, and have been subdivided previously into formae speciales Recent phylogenetic analysis has revealed that formae speciales correspond to biologically and phylogenetically distinct species

Disease symptoms
Typically, FSSC causes foot and/or root rot of the infected host plant, and the degree of necrosis correlates with the severity of the disease Symptoms on above-ground portions of the plant can vary greatly depending on the specific FSSC pathogen and host plant, and the disease may manifest as wilting, stunting and chlorosis or lesions on the stem and/or leaves

Control
Implementation of agricultural management practices, such as crop rotation and timing of planting, can reduce the risk of crop loss caused by FSSC If available, the use of resistant varieties is another means to control disease in the field

Useful websites
http://genomejgi-psforg/Necha2/Necha2homehtml

The Fusarium solani species complex: ubiquitous pathogens of agricultural importance

Nuclear migration, nucleokinesis and lissencephaly

It has long been known that microtubule depletion causes axons to retract in a microfilament-dependent manner, although it was not known whether these effects are the result of motor-generated forces on these cytoskeletal elements. Here we show that inhibition of the motor activity of cytoplasmic dynein causes the axon to retract in the presence of microtubules. This response is obliterated if microfilaments are depleted or if myosin motors are inhibited. We conclude that axonal retraction results from myosin-mediated forces on the microfilament array, and that these forces are counterbalanced or attenuated by dynein-mediated forces between the microfilament and microtubule arrays.

/pdf/motor-proteins-regulate-force-interactions-between-3sjj7e19xi.pdf

Motor proteins regulate force interactions between microtubules and microfilaments in the axon.

This is the publisher's version, also available electronically from "http://www.molbiolcell.org".

https://kuscholarworks.ku.edu/bitstream/handle/1808/17459/Oakley_MBC_11(1)1225.pdf?sequence=1

A Mutation in γ-Tubulin Alters Microtubule Dynamics and Organization and Is Synthetically Lethal with the Kinesin-like Protein Pkl1p

A. THE CENTRAL QUESTION POLARIZED SECRETION 2 B. THE SPITZENKORPER 3 1. Organizer of vesicle traffic 3 2. The Spitzenkorper as a Vesicle supply Center (VSC) 4 3. Spitzenkorper Trajectory 6 4. Growth Pulses and Satellite Spitzenkorper 6 5. Spitzenkorper origin 7 6. Questions 7 C. THE CYTOSKELETON 8 1. Actin Cytoskeleton 8 2. Microtubular cytoskeleton 9 3. Questions 9 D. TURGOR 10 1. Evolutionary and Ecological Significance 10 2. Role of Turgor in Hyphal Growth and Morphogenesis 11 3. Question 12 III. MODELS OF HYPHAL TIP GROWTH 13

Hyphal tip growth: outstanding questions

Cytoplasmic dynein is a microtubule-associated motor protein with several putative subcellular functions. Sequencing of the gene (DHC1) for cytoplasmic dynein heavy chain of the filamentous ascomycete, Nectria haematococca, revealed a 4,349-codon open reading frame (interrupted by two introns) with four highly conserved P-loop motifs, typical of cytoplasmic dynein heavy chains. The predicted amino acid sequence is 78.0% identical to the cytoplasmic dynein heavy chain of Neurospora crassa, 70.2% identical to that of Aspergillus nidulans and 24.8% identical to that of Saccharomyces cerevisiae. The genomic copy of DHC1 in N. haematococca wild-type strain T213 was disrupted by inserting a selectable marker into the central motor domain. Mutants grew at 33% of the wild-type rate, forming dense compact colonies composed of spiral and highly branched hyphae. Major cytological phenotypes included (1) absence of aster-like arrays of cytoplasmic microtubules focused at the spindle pole bodies of post-mitotic and interphase nuclei, (2) limited post-mitotic nuclear migration, (3) lack of spindle pole body motility at interphase, (4) failure of spindle pole bodies to anchor interphase nuclei, (5) nonuniform distribution of interphase nuclei and (6) small or ephemeral Spitzenkorper at the apices of hyphal tip cells. Microtubule distribution in the apical region of tip cells of the mutant was essentially normal. The nonuniform distribution of nuclei in hyphae resulted primarily from a lack of both post-mitotic nuclear migration and anchoring of interphase nuclei by the spindle pole bodies. The results support the hypothesis that DHC1 is required for the motility and functions of spindle pole bodies, normal secretory vesicle transport to the hyphal apex and normal hyphal tip cell morphogenesis.

Role of fungal dynein in hyphal growth, microtubule organization, spindle pole body motility and nuclear migration

An astral pulling force helps to elongate the mitotic spindle in the filamentous ascomycete, Nectria haematococca. Evidence is mounting that dynein is required for the formation of mitotic spindles and asters. Obviously, this would be an important mitotic function of dynein, since it would be a prerequisite for astral force to be applied to a spindle pole. Missing from the evidence for such a role of dynein in aster formation, however, has been a dynein mutant lacking mitotic asters. To determine whether or not cytoplasmic dynein is involved in mitotic aster formation in N. haematococca, a dynein-deficient mutant was made. Immunocytochemistry visualized few or no mitotic astral microtubules in the mutant cells, and studies of living cells confirmed the veracity of this result by revealing the absence of mitotic aster functions in vivo: intra-astral motility of membranous organelles was not apparent; the rate and extent of spindle elongation during anaphase B were reduced; and spindle pole body separation almost stopped when the anaphase B spindle in the mutant was cut by a laser microbeam, demonstrating unequivocally that no astral pulling force was present. These unique results not only provide a demonstration that cytoplasmic dynein is required for the formation of mitotic asters in N. haematococca; they also represent the first report of mitotic phenotypes in a dynein mutant of any filamentous fungus and the first cytoplasmic dynein mutant of any organism whose mitotic phenotypes demonstrate the requirement of cytoplasmic dynein for aster formation in vivo.

A cytoplasmic dynein required for mitotic aster formation in vivo

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Role of fungal dynein in hyphal growth, microtubule organization, spindle pole body motility and nuclear migration

A cytoplasmic dynein required for mitotic aster formation in vivo