PurposeTo report a case of aniridia in a pseudophakic patient following blunt trauma to the eye.Case reportThe traumatized eye had cataract surgery through a 3.0 mm clear corneal incision 6 years prior to the incident. While there have been previous cases of traumatic aniridia in pseudophakic eyes, previous reports have all occurred closer to the time of the cataract surgery. We believe that the most likely mechanism of loss of iris tissue is through wound dehiscence, which would suggest the relative instability of clear corneal incisions several years postoperatively. The patient’s visual acuity returned to 20/20 4 weeks post-trauma, with symptoms of glare which were managed by the use of a colored contact lens.ConclusionThe possibility of wound dehiscence should be recognized as an important clinical entity in the immediate postoperative period, but also several years following cataract surgery.

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Glutamine is the preferred source of nitrogen of Neurospora crassa. In its presence and that of the gene product of MS5 (nmr-1), the fungus represses the assimilation of less preferred forms of nitrogen, such as nitrate. In the absence of glutamine and the presence of the product of gene nit-2, less preferred forms of nitrogen are assimilated as long as a specific pathway for their assimilation is induced. We report here the isolation, from a cosmid bank, of a gene that complements MS5 and can also complement nit-2. We speculate that this result suggests an interaction between the MS5 and nit-2 gene products and that this is important in the regulation of nitrate assimilation.The assimilation of nitrate is a highly regulated process in ascomycetes (13,18,20). The product of gene nmr-J (Fungal Stock Collection no. 3931, Fungal Genetics Stock Center [FGSC], Department of Microbiology, University of Kansas Medical Center, Kansas City, Kans.; allelic with MS5 FGSC 4504) in the presence of glutamine is thought to repress transcription of the structural genes for nitrate reductase (nit-3) and nitrite reductase (nit-6) and of genes controlling a number of other nitrogen-scavenging metabolic pathways in Neurospora crassa (7,16,17). The product of gene nit-2 (FGSC 982, 983) of N. crassa turns on nitrogen-scavenging metabolic pathways in the presence of a pathway-specific inducer and a positive effector when glutamine is absent from the medium (13,20). In the case of the assimilation of nitrate in N. crassa, the specific inducer is nitrate or nitrite (13,20), and the metabolic pathway-specific effector is the product of gene nit4 (nit-5 and nit4 are probably allelic) (13).In Aspergillus nidulans there is a similar system, but, unlike the situation in N. crassa, no mutations in a gene equivalent to nmr-J have been found, suggesting to Marzluf and Fu (G. from ours but presumably contains the same gene. Preliminary reports of both Marzluf's and our work have appeared in the abstracts of the 16th International Genetics Congress in Toronto, Ontario, Canada, 20-27 August 1988.) Isolation of a cosmid that complements nonrepressible nmr-1 and MS5 mutant strains. Nitrate reductase reduces nontoxic chlorate to toxic chlorite; hence, nitrate reductasecontaining Neurospora cells commit suicide on chloratecontaining medium. The synthesis of nitrate reductase is repressed in the presence of adequate leVels of glutamine in wild-type Neurospora cells; hence, on glutamine-plus-chlorate-containing medium, wild-type Neurospora cells will survive. The wild-type allele of MS5 (nmr-J) is needed for the repression by glutamine of the synthesis of nitrate reductase; hence, strains mutated in this gene will commit suicide on medium containing glutamine plus chlorate, unlike their wild-type or complemented counterparts. The Neurospora genomic library of Vollmer and Yanofsky (19) was made in cosmid pSV50, which contains a benomyl resistance gene. This library was screened by making DNA minipreparations (4, 10) of each entry, pooling equal porti...

Glutamine is the preferred source of nitrogen of Neurospora crassa. In its presence and that of the gene product of MS5 (nmr-1), the fungus represses the assimilation of less preferred forms of nitrogen, such as nitrate. In the absence of glutamine and the presence of the product of gene nit-2, less preferred forms of nitrogen are assimilated as long as a specific pathway for their assimilation is induced. We report here the isolation, from a cosmid bank, of a gene that complements MS5 and can also complement nit-2. We speculate that this result suggests an interaction between the MS5 and nit-2 gene products and that this is important in the regulation of nitrate assimilation.