What effect does the Barr body have, in relation to female Turner syndrome?
The reason is that X-inactivation is not complete (Carrell &amp; Willard, 2005; Ahn &amp; Lee, 2008), and as many as 15-25% of X-linked genes escape silencing (Carrell &amp; Willard, 2005; Cheng et al, 2005). This means that some genes on the Barr body are expressed in XX-females, although often at lower levels compared to the active X-chromosome, and this is part of the normal gene dosage. The "purpose" of X-inactivation is usually dosage compensation, so that genes are expressed equally in males and females (and then actually upregulated in both sexes to balance autosomal genes, see e.g. Dementyeva et al, 2009). However, this is not true for all genes, and the ones that normally escape X-inactivation will be expressed in the incorrect dosage in X0 females. Some of these genes are thought to contribute to the symptoms of Turner syndrome.

It is also likely that the genes that escape silencing are involved in sex-linked traits, as stated in Carrell &amp; Willard (2005):


  Such genes are potential contributors to sexually dimorphic traits, to phenotypic variability among females heterozygous for X-linked conditions, and to clinical abnormalities in patients with abnormal X chromosomes.
  ... ...
  However, as many of the genes that escape from inactivation do not have Y-linked homologues, strict dosage compensation may not be necessary for all genes on the chromosome. Such characteristic genomic differences should be recognized as a factor for explaining sex-specific phenotypes both in complex disease as well as in normal, sexually dimorphic traits.


Cheng et al (2005) also point out that the expression of the genes that escape silencing is tissue-dependent, which suggests that the role these genes play in the symptoms of Turner syndrome is also tissue dependent.