<p class="MsoNormal"><span> </span>Two adjacent posterior Hox genes in C. elegans,
nob-1 and
php-3, are both required for normal male tail development, based on experiments with the deletion alleles
nob-1(
ct230) (loss-of-function) and
php-3(
ok919) (probable null).<span> </span>In hermaphrodites, the
nob-1 mutation causes posterior defects (see below), but the
php-3 mutation has no obvious effect.<span> </span>In males, however, the two mutations cause similar male tail abnormal (Mab) phenotypes including ray defects, as well as inability to mate.<span > </span>The two genes appear to interact: RNAi of either one in the mutant background of the other causes more severe Nob (No back end) and Mab phenotypes.<span> </span>However, their functions are not completely overlapping: the <i >
php-3(
ok919) Mab phenotype could not be rescued by a
nob-1 construct, lacking the
php-3 gene, that rescues
nob-1(
ct230), suggesting that
php-3 function cannot be supplied by over-expression of
nob-1.<span> </span>The
php-3 Mab phenotype could not be rescued by a construct including the <i >
php-3 gene and most of the upstream
nob-1 gene including its large second intron.<span> </span>However, it could be partially rescued by a similar construct that carried 2.8 kb of the
nob-1 promoter region and a
nob-1 gene inactivated by a nonsense mutation, implying that
php-3 expression is dependent on elements in the
nob-1 regulatory region.A rescuing
nob-1::GFP construct including 10 kb of upstream sequence is expressed in several L1 tail cells, including vir<span> </span>(Intestino-rectal valve), the anal sphincter cell, and tail hypodermal cells. Accordingly, many <i >
nob-1(
ct230) adult hermaphrodites have rectal defects (constipation) and abnormal tail tips.<span> </span>Truncated constructs with promoters as short as 0.5 kb drive expression in a similar pattern, but could no longer rescue the <i >
nob-1(
ct230) phenotype.<span> </span>The expression pattern of
php-3 is currently under investigation.Yeast two hybrid experiments revealed an apparent strong interaction between NOB-1 and NIH-1 (K10D6.4), which also interacts with several other Hox gene products expressed in the male tail and can mutate to cause a Mab phenotype (R. Hong, personal communication).<span> </span>Possible functions of this interaction are being investigated.</span>