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Comments on Bork JA et al. (1995) International C. elegans Meeting "Gon(q7) DISRUPTS FORMATION OF THE SOMATIC GONADAL PRIMORDIUM AND APPEARS TO LACK DISTAL TIP CELL" (0)
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Bork JA, Ellis RE, & Kimble JE (1995). Gon(q7) DISRUPTS FORMATION OF THE SOMATIC GONADAL PRIMORDIUM AND APPEARS TO LACK DISTAL TIP CELL presented in International C. elegans Meeting. Unpublished information; cite only with author permission.
The somatic gonad is a complex organ with several distinct cell types and tissues. During L1 and L2, two progenitor cells, Z1 and Z4, generate the 10-celled (male) or 12-celled (hermaphrodite) somatic gonadal primordium. Subsequently, during L3 and L4, the somatic gonadal primordium develops into the major tissues of the somatic gonad. To analyze genetic controls of early gonadogenesis, we have focused on the Gon(q7) mutation (see also abstract by Santa Anna-Arriola et al.). Gon(q7) is an EMS-induced, recessive mutation that maps close to fog-3 on LGI. Although Gon(q7) disrupts gonadogenesis in both hermaphrodites and males, we have focused on hermaphrodites. By Nomarski, the somatic gonad of Gon(q7) animals is small and grossly misshapen: most possess spermathecal and uterine tissues, but these tissues are not properly organized. Little, if any, arm extension is seen, and few germ cells are generated. Sperm are usually observed, but few contain oocytes. A vulva is usually present. The lack of arm extension and the low abundance of germ cells in Gon(q7) gonads suggested to us that the distal tip cells (Z1.aa and Z4.pp) may be missing. Consistent with this idea, expression of lag-2::lacZ , a distal tip cell marker [1], is not observed. Our current hypothesis, supported by preliminary lineage studies, is that Z1.aa and Z4.pp may adopt a new fate in Gon(q7) mutants. That new fate may involve production of more spermathecal and uterine cells. Both by Nomarski and using UL8, a lacZ construct expressing in spermathecae, uterus, and rectal valve cells (I. Hope, personal communication), Gon(q7) gonads appear to have an excess of spermathecal and/or uterine tissue. Gon(q7) has been carefully mapped by 3-factor crosses and deficiency-mapping, including single-egg PCR. Recently, we obtained cosmid rescue of Gon(q7) and we are now trying to obtain smaller rescuing fragments. Also, we are screening for additional alleles using a non-complementation screen in an attempt to identify null alleles.